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 +9  (nbme24#3)

The most direct path, and most likely path, for breast cancer to metastasize to the vertebra are the intercostal veins. This was on an earlier NBME test as well. Breast cancer will cause mixed, lytic and blastic lesions once in bone.

On an unrealated note; I finally came up with a decent way to remember lytic vs. blastic cancers in bone!

kIdneY and thYroId cause lYtIc

prostate > blastate > blastic

Two breasts > two types of lesions > B reast causes B oth

Two lungs > two types of lesions (depending on type of lung cancer)

small-cell lung > "small blasts"

non-small cell > lytic

artist90  VEINS: 1-Intercostal veins drain into Azygous vein which drains into SVC BUT some blood from this Azygous vein is also draining into BATSONS VERTEBRAL VENOUS PLEXUS how the breast cancer metastasizes to vertebral column. 2-Internal thoracic(mammary) vein drains directly into Brachiocephalic vein. 3-Lateral thoracic vein drains into Axillary vein which drains into Subclavian vein which drains into Brachiocephalic vein. ARTERIES ARE DIFFERENT: Subclavian artery----branches into---Internal thoracic(mammary) artery---Intercostal arteries. Internal thoracic artey is used for CABG if there is 1 vessel block.

 +11  (nbme24#16)

Flexor digitorum profundus is responsible for flexion of DIP. Medial aspect of the muscle (which flexes the 4th and 5th digit) is supplied by the ulnar nerve (C8, T1). The lateral aspect (which flexes the 2nd and 3rd digit) is innervated by the median nerve specifically the anterior interosseous branch (C8, T1). So the question is describing a laceration damaging the nerve supply to the DIP flexor of the 2nd digit (index finger). This is saying the medial nerve is being damaged (C8 and T1; lower trunk roots).

Lumbricals (1st/2nd, median; 3rd/4th, ulnar) are a group of muscles that flex at the MCP joint, and extend PIP and DIP joints.

Could remember as 'flexor digitorum profundus is profoundly long' since tendons insert on DIPs. Compared to flexor digitorum superficialis whose tendon wraps around profundus' superficially but inserts on PIPs.

toupvote  This is dumb but I remember FDP is needed for picking while FDS is need for scratching the superficial layer of the skin
whoissaad  @lsmarshall Flexor digitorum superficialis inserts at the middle phalanges to be more specific.

 +8  (nbme24#27)

"Parasternal heave (lift) occurs during right ventricular hypertrophy (i.e. enlargement) or very rarely severe left atrial enlargement." RV hypertrophy can be seen so easily because the RV is at the anterior surface of the chest.

In this patient blood from LA to LV decreases in saturation, so it is going somehwere. From the O2 sat. we can deduce there is probably a VSD (increased RV pressure would cause RVH and parasternal heave). Furthermor, the vignette is likely describing tetralogy of fallot (caused by anterosuperior displacement of the infundibular septum). In Tet spells, RV outflow is too obstructed and patient gets cyanosis and R>L shunting Squats increase SVR, decreasing R>L shunting, putting more blood through pulmonary circuit and relieving cyanosis.

seagull  i'm pretty sure your a prof and not a student.
nor16  nevertheless, we are greatful for explanation!
niboonsh  I remember seeing a question describe parasternal lift in the context of pulm htn. still got this wrong tho fml

 +14  (nbme24#20)

Patient has Spina bifida occulta which is a neural tube defect (failure of fusion of the neuropores). Sclerotomes are the part of each somite in a vertebrate embryo giving rise to bone or other skeletal tissue. Since a part of this patient's spina bifida included "abscense of spinous process" then a sclerotome was involved. Knowing that neural tube defects are an issue with fusion should be enough to get to the right answer.

If the notochord failed to develop then the entire CNS would not develop as the notochord induces formation of neural plate.

If the neural tube failed to develop then the whole CNS would not have developed.

Yolk sac is irrelevant to this patient.

When neural crest cell it has different outcomes in different tissues. Failure of neural crest to migrate in heart can cause Transposition of great vessels, Tetralogy of Fallot, or Persistent truncus arteriosus. Failure of neural crests to migrate in GI can cause Hirschsprung disease (congenital megacolon). Treacher Collins Syndrome can occur when neural crest cells fail to migrate into 1st pharyngeal arch. Neural tube defects has nothing to do with failure of neural crest migration though.

sympathetikey  Exactly. I knew it had to due with fusion of the neuropores but had never heard of sclerotomes. Thanks for the explanation.

 +5  (nbme24#8)

"The exact mechanism for tremor induction by β(2)-adrenergic agonists is still unknown, but there is some evidence that β(2)-adrenergic agonists act directly on muscle... More recently, tremor has been correlated closely with hypokalaemia." - NIH publication

First Aid mentions hyperthyroidism causing tremor from β-adrenergic stimulation. It also mentions β2-agonists causing tremor as a side effect. First Aid also mentions β2-agonists driving potassium into cells, which may contribute to tremor. That said, more classic symptoms of hypokalemia are wide QRS and peaked T waves on ECG, arrhythmias, and muscle weakness.

Looking around on the internet looks like if therapy is continued the tremor from a β2-agonists resolves overtime.

xxabi  Sketchy mentions tremor and arrhythmia as side effects!

 +7  (nbme24#1)

An experimental design or experimental study must have an intervention, by definition. Case-control studies are observational studies, not experimental. This question is technically incorrect. They wanted to amke a point that case-control studies are time and cost efficient since they don't require following patients over time or any resources besides reviewing/gathering information. Case series could not test this hypothesis.

Also, the wording "associated wit an increased risk" somewhat alludes to case-control studies only having the ability to find odds of an associations between exposure and outcome, but not establish causal relationship.

bigjimbo  classic nbme

 +5  (nbme24#35)

"Desmosome (Macula adherens) - A cell-to-cell connection that provides structural support with intermediate filaments, particularly in tissues that undergo mechanical stress (e.g., skin, gastric tissue, bladder). Connects keratinocytes in the stratum spinosum of the epidermis." - AMBOSS

sympathetikey  This is why I was looking for some answer indicating keratinocytes in the stratum spinosum...instead they just gave a bunch of bs choices.
roygbiv  I'm confused because I also know that S. aureus cleaves desmoglein in the stratum granulosum, so why is it specifically this answer?
duat98  desomosomes connects cells to cells. hemidesmosome connects cells to basement membrane.

 +5  (nbme24#27)

Polyneuropathy - A condition involves damage to multiple peripheral nerve fibers. Patients typically present with symmetric distal sensory loss or a burning sensation associated with motor weakness. Classic polyneuropathy is burning so this question was more process of elimination. Others did not fit well.


 +4  (nbme24#33)

Inhalant abuse could be done with glue, paint thinners, fuel, nitrous oxide, or alkyl nitrites. Usually in high-school aged kids. Inhalants are 'downers' so whatever intoxication effects there are should be depressant and fully resolve within 30 min. to a couple hours. Patients may look drunk when intoxicated with inhalants, but usually quickly resolve. A characteristic "glue sniffer's rash" around the nose and mouth is sometimes seen after prolonged use.


 +7  (nbme24#48)

PCA stroke can cause "prosopagnosia" which is the inability to recognize familiar faces. Caused by bilateral lesions of visual association areas, which are situated in the inferior occipitotemporal cortex (fusiform gyrus). The ability to name parts of the face (e.g., nose, mouth) or identify individuals by other cues (e.g., clothing, voices) is left intact.

Without knowing that, remembering occipital lobe is involved in 'visual stuff' broadly, including image processing and this patient is having issues with understanding images should be enough to get to the answer.

gonyyong  Lol I guessed it exactly because of that
sympathetikey  Never heard of that one before. Thanks!
karthvee  This is not prosopagnosia, but instead a case of apperceptive agnosia. Wiki: "...patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch." Although, lesions tend to be in the occipito-parietal area so PCA again is the answer!

 +15  (nbme24#8)

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia
seagull  i'm leaning towards Ornithine transcarbamylase deficiency.
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria?
charcot_bouchard  if it was mitochondrial disorder no one would escape
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine?
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld)
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA.

 +3  (nbme24#37)

"Air droplets" sounds like respiratory (saliva or water) droplets. Inhalation of toxoplasma oocysts in cat feces isn't quite the same; not to say I know exactly what the oocysts are inhaled as (just microscopic dry cat poop particles?). Ingestion of undercooked meat to get the cysts is certainly a ROT for toxoplasma.

Toxoplasma as TORCH has triad of hydrocephalus, cerebral calcifications (intracerebral), and chorioretinitis. chorioretinitis can be in congenital CMV or toxoplasmosis. Periventricular calcifications are in CMV. Congenital CMV usually has hearing loss, seizures, petechial rash, “blueberry muffin” rash, chorioretinitis, and periventricular calcifications.

usmile1  also note that toxoplasma can cause the "blueberry muffin" rash (also rubella can as well)

 +16  (nbme24#49)

Androgen Insensitivity Syndrome - Defect in androgen receptor resulting in normal-appearing female (46,XY DSD). Functioning testes causes increased testosterone at puberty, which is converted to estrogen peripherally, giving female secondary sexual characteristics (female external genitalia). Lack of androgen receptor function leads to absent or scant axillary and pubic hair. Patients have rudimentary vagina, but uterus and fallopian tubes absent.

Androgen insensitivity syndrome is the answer but you might have considered Müllerian agenesis (Mayer-Rokitansky- Küster-Hauser syndrome).

Mullerian agenesis will have normal hormone levels and may present as 1° amenorrhea (due to a lack of uterine development) in females with fully developed 2° sexual characteristics (functional ovaries). Hair development is normal as well. Patients also have normal height.

Seems like this question did not give us much to distinguish besides height and tanner stage 1 pubic/axillary hair.

dbg  100% agreed. Mullerian agenesis was on my mind too. The full breast development kept me fixed at this dx. Did not think how high testosterone at this age and insensitivity would push towards peripheral conversion to estrogen and hence breast development. Thanks.

 +8  (nbme24#45)

MHC class 1 peptide antigen processing > "Antigen peptides loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)" - First Aid 2019.

Bare lymphocyte syndrome type 2 (BLS II; affecting MHC II) is due to mutations in genes that code for transcription factors that normally regulate the expression (gene transcription) of the MHC II genes. Bare lymphocyte syndrome type 1 (BLS I; affecting MHC I), is much more rare, and is associated with TAP deficiencies.


 +10  (nbme24#22)

Zellweger syndrome - autosomal recessive disorder of peroxisome biogenesis due to mutated PEX genes. Hypotonia, seizures, hepatomegaly, early death (within 1 year). β-oxidation of VLCFA happens in peroxisomes so the child seemingly having some sort of congenital metabolic disorder with elevated VLCFAs should have been enough to get the answer without knowing about Zellweger.


 +10  (nbme24#25)

Acral lentigious is most common type of melanoma in African Americans and is on the palms or soels. I guess the typical thinking of chest and back (sun exposed) is a little different in this type? Among all demographics; melanomas occur the majority of time on the limbs (~36% lower and ~19% upper); trunk is ~27%... So based on that and him being of African descent we can choose palms.


 +5  (nbme24#1)

Although Crohn's may have ulcers, fistulas, and bleeding; it usually does not cause iron deficiency anemia and has less bleeding than UC. "Structural abnormalities of the terminal ileum, such as Crohn disease and surgical resection, can cause decreased absorption of vitamin B12." - First Aid General Principles


 +2  (nbme24#24)

"Probenecid and high-dose salicylates inhibit reabsorption of uric acid in proximal convoluted tubule (also inhibits secretion of penicillin)." - First Aid 2019

uslme123  so ...............
adisdiadochokinetic  So probenecid is the best answer here because they only specified acetylsalicylic acid, not the dosage, and low-dose acetylsalicylic acid has the opposite effect.

 +3  (nbme24#31)

Filgrastim (G-CSF) is very commonly tested this way; UWorld and elsewhere. Chemo. patient with bone marrow surpression > give G-CSF.


 +5  (nbme24#50)

Metaplasia - A reversible adaptive response in which there is "Reprogramming of stem cellsŽreplacement of one cell type by another that can adapt to a new stress." Both are normal cells. Respiratory tree should not have squamous cells until respiratory bronchioles (before that; cuboidal in term. bron. > columnar in bronch. > pseudostratified columnar in large. bronch.).

shayan  if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal?
artist90  i got it confused bc the question stated that there was a mass in one lobe of lung and i didn't knew that squamous metaplasia also presents as a mass in lung. i missed that on biopsy they were clearly stating squamous metaplasia.

 +7  (nbme24#8)

Synaptobrevin is the target of tetanospasmin (tetanus toxin); muscle spasms are characteristic. Only other answer you might consider is Acetylcholinesterase since he is a farmer and buzzwords often carry us to the promised land... but symptoms of a cholinergic storm are absent.

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know.
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam
yotsubato  Oh and they read FA and did UW to make sure its not in there either
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions!

 +7  (nbme24#33)

"In the years preceding physical puberty, Robert M. Boyar discovered that the gonadotropin pulses occur only during sleep, but as puberty progresses they can be detected during the day. By the end of puberty, there is little day-night difference in the amplitude and frequency of gonadotropin pulses.

Some investigators have attributed the onset of puberty to a resonance of oscillators in the brain.[89][90][91] By this mechanism, the gonadotropin pulses that occur primarily at night just before puberty represent beats." - Wiki

linwanrun1357  Who can explain, the 12-y boy with stanner stage 2?? I thought it should be stage 3....

 +4  (nbme24#22)

I thought this was a trick question since skin cancers are the most common type of cancers overall. But actually among HIV patients, HIV-related cancers are much more common than non-HIV-related cancers (even skin cancers). EBV-induced primary CNS lymphoma is the only option that is AIDs-defining illness/cancer.

medskool123  why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this?
haliburton  Yes, I think CNS lymphoma as an AIDS defining illness wins the day. My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?)
yotsubato  God damn this is such BULLSHIT...
trichotillomaniac  Why you gotta do me dirty like this NBME

 +7  (nbme24#11)

Monozygotic ("identical") twins have 50% of getting schizophrenia if their twin has it. Dizygotic twins have ~ 20% chance though. This is often mentioned when Schizophrenia etiology is discussed (i.e., we don't know but concordance studies suggest a genetic link). T1DM has less of a genetic link than T2DM but it also has 50% concordance between monozygotic twins. This fact is mentioned in First Aid 2019, page 346... I got this NBME question wrong but it's content is in board sources.





Subcomments ...

submitted by medstudied(2),

Can someone explain why the correct answer for the question here is conjugation but can’t be transposition?

catacholamine16  Transposition is when a segment of DNA (in this case, coding for resistance) jumps onto a plasmid within the same bacterial cell. That plasmid might then transfer to another nearby bacterial cell via conjugation. Transposition is happening WITHIN the bacterium. Conjugation is how that resistance gene gets transferred. +1  
lsmarshall  Also, E. coli is the classic example of a bug tat uses conjugation. ^but explanation above is correct^ +1  
seagull  I think he might have did what I did. I got Transformation mixed up with transposition. FML +2  


submitted by sattanki(31),

Apparently there is a completely separate spinal cord reflex where direct penile stimulation leads to an erection. This reflex only needs an intact arc in S2-S4, so as long as this region is not injured, an erection can still occur. However, with transection at C8, then the psychogenic erection reflex cannot occur, as this requires descending fibers from the cortex.

lsmarshall  Just saw a good summary of nerves/vessels involved saying, "pelvic parasympathetic fibers from S2-S4 can cause cavernous arteriole vasodilation via the cavernous nerve without of central stimulation." +3  
seagull  S2-3-4 keeps the penis off the floor +9  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +  


Why do you give IV leucovorin with intrathecal methotrexate? Wouldn’t MTX lose its efficacy since leucovorin reverses the effects of MTX?

colonelred_  MTX will still work but yes some purine/pyrimidine synthesis can still occur. You often give leucovorin to decrease adverse effects of MTX. +  
welpdedelp  ok I have a question, leucovorin is the same as folic acid...so why give one over the other? +  
lsmarshall  Leucovorin, folinic acid, is a modified version of THF and enter folate metabolism where THF is, after the point where methotrexate takes its effect. I have a pharm. card that says "toxic effects on normal cells may be reduced by administration of folinic acid (a.k.a. leucovorin or citrovorum factor), which is **preferentially taken up by normal cells versus tumor cells**." +2  


submitted by lsmarshall(191),

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +3  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +1  
charcot_bouchard  if it was mitochondrial disorder no one would escape +  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +1  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +3  


lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +5  
famylife  "When a rectocele becomes large, stool can become trapped within it, making it difficult to have a bowel movement or creating a sensation of incomplete evacuation. Symptoms are usually due to stool trapping, difficulty passing stool, and protrusion of the back of the vagina through the vaginal opening. During bowel movements, women with large, symptomatic rectoceles may describe the need to put their fingers into their vagina and push back toward the rectum to allow the stool to pass (“splinting”). Rectoceles are more common in women who have delivered children vaginally." https://www.fascrs.org/patients/disease-condition/pelvic-floor-dysfunction-expanded-version +5  
usmleuser007  really like the pubic hair.... +