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 +4  (nbme23#28)

To be completely clear!

This patient has Cystinosis a rare autosomal recessive lysosomal storage disorder and most common cause of Fanconi syndrome in children. Cystinosis is systemic and leads to cystine crystal deposits in cells and tissues throughout the body.

Although Wilsons disease can lead to FS, the crystals in the corneas does not correlate with Wilsons disease.
More info: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841061/


 +2  (nbme23#14)

Mucor, Rhizopus, Absidia (Zygomycophyta) Irregular, broad, nonseptate hyphae branching at wide angles. Sporangiospores are inhaled from soil. The fungi penetrate the cribiform plate (no barriers), proliferate in blood vessel walls, progressing rapidly from sinuses into the brain tissue. • Mucormycosis: Rhinocerebral, frontal lobe abscess; cavernous sinus thrombosis. Characterized by paranasal swelling, necrotic tissues (black necrotic eschar on face), hemorrhagic exudates from nose and eyes, mental lethargy, headache, facial pain; may have cranial nerve involvement. • Occurs in ketoacidotic diabetic and neutropenic (leukemic) patients Treatment: debridement of necrotic tissue and amphotericin B or isavuconazole started immediately. Fatality rate is high due to rapid growth and invasion.

jboud86  FA 2019 page 153.




Subcomments ...

submitted by yb_26(43),

abnormal test result means that test detects cancer =>

  • 35 of 50 men with prostate cancer have abnormal test result => n of pts with cancer = 50. Test shows cancer in 35 men => TP=35 => we can calculate FN = 50-35 = 15

  • 20 of 100 men without prostate cancer have abnormal test results => FP =20 => we can calculate TN = 100-20=80

  • now we can calculate specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%)

here is my 4/4 table: [https://www.reddit.com/r/usmlestep1/comments/ccul3w/biostat_question_from_nbme23/]

smc213  Exactly what I did! +  
smc213  I googled the meaning of abnormal test results just to make sure. A positive test is one in which the result of the test is abnormal; a negative test is one in which the test's result is normal. +  


submitted by yb_26(43),

abnormal test result means that test detects cancer =>

  • 35 of 50 men with prostate cancer have abnormal test result => n of pts with cancer = 50. Test shows cancer in 35 men => TP=35 => we can calculate FN = 50-35 = 15

  • 20 of 100 men without prostate cancer have abnormal test results => FP =20 => we can calculate TN = 100-20=80

  • now we can calculate specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%)

here is my 4/4 table: [https://www.reddit.com/r/usmlestep1/comments/ccul3w/biostat_question_from_nbme23/]

smc213  Exactly what I did! +  
smc213  I googled the meaning of abnormal test results just to make sure. A positive test is one in which the result of the test is abnormal; a negative test is one in which the test's result is normal. +  


submitted by mousie(83),

Can someone please explain this to me? I don't understand why starting the other drug would not count as exclusion criteria?

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +7  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +3  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +  
yex  I agree with @notadoctor !! +  


Patient is current breast-fed, so we can eliminate fructose (fructose is found in honey and fruits and some formula, but not in breast milk). Patient has reducing substances but no glucose in the urine, so he must some non-glucose sugar. My differential for reducing non-glucose sugars in the urine is disorders fructose metabolism or galactose metabolism. We have eliminated fructose, so that leaves us with galactokinase deficiency or classic galactosemia.

sympathetikey  & Galactokinase deficiency would be much milder. +3  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +  


The key is the free air in the abdominal cavity. Ulcers, especially duodenal ulcers, can perforate into the abdominal cavity. This can cause a pneumoperitoneum (free air under the diaphragm). Not a listed symptom in this question, but this can also cause referred pain to the shoulder by irritating the phrenic nerve. FA 2019 pg 374

et-tu-bromocriptine  To add on to this, anterior* duodenal ulcers tend to perforate (makes sense because closest to the abdominal cavity) whereas posterior duodenal ulcers tend to bleed (due to proximity to the gastroduodenal artery). +1  
smc213  Acute pancreatitis can also occur with a posterior duodenal ulcer rupture. Source: Pathoma +1  


I thought of this as squamous cell carcinoma of the lung causing increased PTHrP and hypercalcemia.

d_holles  I thought this was medullary thyroid cancer but demographically SCC works better. +  
smc213  Medullary thyroid carcinoma increases calcitonin levels leading to decreased serum Ca2+ by increasing Ca2+ renal excretion. So high levels of calcitonin secreted by the tumor may lead to hypOcalcemia. Source: Pathoma +5  


submitted by mguan1993(2),

Does being recently diagnosed vs having CKD for a while change this answer? the "recently diagnosed" part threw me off

smc213  @mguan1993 yes it does! With secondary hyperPTH due to CKD = incr. phosphate, dec. Ca2+ and incr. PTH. This can then progress to tertiary hyperPTH from longstanding secondary hyperPTH as a result of parathyroid HYPERPLASIA --> autonomously (refractory) functioning parathyroid. This will actually lead to INCREASED Ca2+, and significantly INCREASED PTH. Treatment would be surgical removal of the parathyroid glands. Sources: DIT and FA18 p340 +1  


What puts internal rotation over adduction? Subscapularis muscle does both

smc213  probably because the subscapularis m. is the only SITS muscle that does internal rotation & adduction along with the teres minor m. action being adduction & external rotation. +  


submitted by mousie(83),

Cholera = Fecal oral /Legionnaires = Legonalla pneumo = NO person to person only by inhalation of bacteria contaminated water /Lyme = tick bite /Meningiococcal = sharing respiratory and throat secretions (saliva or spit). Generally, it takes close (for example, coughing or kissing) or lengthy contact to spread these bacteria (CDC) /RMSF = tick bite

smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments. +2  
dentist  So, Cholera is also p2p but Mening is more likely? +  


submitted by gabeb71(15),

Lomustine ia an alkylating nitrosourea compound used in chemotherapy. Alkylating agents crosslink DNA.

Cyclophosphamide metabolizes into a phosphoramide mustard. Phosphoramide mustard forms DNA crosslinks both between and within DNA strands

Cholchicine and Vinblastine work on microtubules

Methotrexate and 5-FU both work on purine metabolism.

Cytosine arabinoside interferes with the synthesis of DNA. Its mode of action is due to its rapid conversion into cytosine arabinoside triphosphate, which damages DNA when the cell cycle holds in the S phase (synthesis of DNA). Rapidly dividing cells, which require DNA replication for mitosis, are therefore most affected.

smc213  To clarify Methotrexate (inhibits dihydrofolate reductase) and 5-FU (inhibits thymidylate synthase) in the Pyrimidine synthesis pathway. 6-MP inhibits Glutamine PRPP amidotransferase in the PURINE synthesis pathway +  


submitted by sajaqua1(202),

Plasma membranes are a lipid bilayer, typically with phosphate heads on each surface and long carbon tails on the inside. These carbons are neutral, and undergo hydrophobic interactions for an energetically favorable state.

Integral membrane proteins pass through this lipid bilayer, and so must be capable of interacting both with the polar solvents of intracellular and extracellular space, as well as the hydrophobic core of the layer. The transmembrane portion often has alpha-helical secondary conformation, with hydrophobic residues like glycine on the outside towards the carbon tails with polar amino acid residues tucked in.



submitted by step420(18),

Integral membrane proteins are found within the plasma membrane and span the whole length across. The inside of the membrane is very hydrophobic due to the long carbon chains. Extensive hydrophobic interactions between the protein side chain and the lipid tails will help anchor the protein in the membrane.

yb_26  O-linked glycosylation of secreted and membrane bound proteins is a post-translational event that takes place in the cis-Golgi compartment after N-glycosylation and folding of the protein +  


usmleuser007  in a per-protocol analysis,[6] only patients who complete the entire clinical trial according to the protocol are counted towards the final results +1  
sympathetikey  "In an ITT population, none of the patients are excluded and the patients are analyzed according to the randomization scheme." +1  
smc213  This video helps https://www.youtube.com/watch?v=Kps3VzbykFQ +2  
rio19111  Thx smc213, really helped. +  


submitted by hayayah(399),

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

smc213  Septic shock can also present with hypothermia <36C +  


submitted by hayayah(399),

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

Small cell may actually produce antibodies against presynaptic Ca channels.

smc213  Increased PTHrP seen in squamous cell lung cancer leads to increased Ca2+ levels +3  


submitted by usmleuser007(113),

Salivary secretion 1. At low flow = High concentration of potassium; low concentrations of sodium, bicarb, & chloride 2. at high flow = low concentration of potassium; high concentrations of sodium, bicarb, & chloride

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me?? +  
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production. +  
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated. +1  


Legionella is common causes of pneumonia superimposed on chronic obstructive pulmonary disease.

asapdoc  Im pretty sure so is strept pneumoniae +2  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +1  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +1  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +1  


how do we know parakeets cause hypersensitivy pneumonitis

smc213  FA18 p.657 bird exposure--> HSN pneumonitis (restrictive lung disease) and FA18 p.214 granulomatous diseases: foreign material-->HSN pneumonitis. I had to make sense of it since I didn't know it was HSN pneumonitis at first. +  


submitted by hayayah(399),

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 =/ +5  
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); +7  
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 hayayah(399),

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 =/ +5  
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); +7  
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 radion(2),

Hypercarbia causes cerebral vasodilation. If you have ever seen an intra- or acute post-op neurosurgical patient, or really any patient about to herniate, you can remember this because they will be hyperventilated to pCO2 around 25-30 to decrease ICP via cerebral vasoconstriction; in this case, we have the opposite. The curve of pCO2 vs cerebral blood flow is quite steep in the physiologic range meaning small changes in ventilation make a significant difference in CBF.

smc213  FA 2018 p.486 +2  


submitted by hayayah(399),

Familial adenomatous polyposis is an autosomal dominant mutation. Thousands of polyps arise starting after puberty; pancolonic; always involves rectum. Prophylactic colectomy or else 100% progress to CRC.

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

sympathetikey  I would say this is Lynch Syndrome (APC is usually thousands of polyps) but lynch syndrome would generally have a family history of other cancers as well, so you might be right. Either way, both autosomal dominant so win win. +1  
smc213  uptodate states: Classic FAP is characterized by the presence of 100 or more adenomatous colorectal polyps +  
dickass  @sympathetikey Lynch Syndrome is literally called "Hereditary NON-POLYPOSIS colorectal cancer" +  


submitted by haliburton(83),

Mycoplasma pneumoniae cold agglutinins, no response to amoxicillin.

FA 2017: Classic cause of atypical “walking” pneumonia (insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate). X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs. Grown on Eaton agar. Treatment: macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since Mycoplasma have no cell wall). ABC = Africa, Blindness, Chronic infection. D–K = everything else. Neonatal disease can be acquired during passage through infected birth canal. No cell wall. Not seen on Gram stain. Pleomorphic A. Bacterial membrane contains sterols for stability. Mycoplasmal pneumonia is more common in patients < 30 years old. Frequent outbreaks in military recruits and prisons. Mycoplasma gets cold without a coat (cell wall).

johnthurtjr  Have you mixed Chlamydia in with Mycoplasma? +  
smc213  I mean the Q stem is not about Chlamydiae, but Chlamydiae does lack the classic PTG cell wall d/t decreased muramic acid = beta-lactam abx ineffective. FA 2018 p.148 +  


submitted by hayayah(399),

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

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

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

missi199  Could I ask why it is not Lysosomal protease +3  
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: https://www.mdpi.com/1999-4915/9/11/322/htm +1  
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc. +2  


submitted by hayayah(399),

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

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

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

missi199  Could I ask why it is not Lysosomal protease +3  
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: https://www.mdpi.com/1999-4915/9/11/322/htm +1  
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc. +2  


I think this one has to do with "late dumping syndrome"-- basically, starchy foods cause hyperglycemia --> release of insulin --> catecholamine surge --> diarrhea, etc.