need help with your account or subscription? click here to email us (or see the contact page)
join telegramNEW! discord
jump to exam page:
search for anything โ‹… score predictor (โ€œpredict me!โ€)

Welcome to an1โ€™s page.
Contributor score: 114


Comments ...

 +0  visit this page (free120#37)
get full access to all content โ‹… become a member

Always be kind! Spending a few extra minutes will make him feel better, solidify your relationship, and not really waste too much of your time. She passed away on this same day, he must be very sad and having someone to talk to can change everything.

get full access to all content โ‹… become a member

 +1  visit this page (free120#26)
get full access to all content โ‹… become a member

Patient had ALS. Combination of UMNL + LMNL --> only answer option that had anything to do with these was atrophy (LMNL). Also, remember that their MCC of death is due to respiratory/ diphragmatic failure!

get full access to all content โ‹… become a member
athenathefirst  Agreed. Right away UMN and LMN signs>>>> ALS the man has Steve Hawkings disease (RIP) . I always think of this amazing man when I think of this disease. +

 +0  visit this page (free120#5)
get full access to all content โ‹… become a member

"pink, soft, granular, edematous wound" describes granulation tissue, which appears around day 3 and last several weeks. At this time, there is also an abundance of fibroblasts, endothelial cells (which contribute to angiogenesis with up regulation of VEGF) and macrophages as well as keratinocytes.

get full access to all content โ‹… become a member

 +0  visit this page (nbme18#32)
get full access to all content โ‹… become a member

I was so lost when I saw this. But I was able to break it down and figure out what's happening.

HOX is transcription from Head (cranial) โ€”> Toe (caudal)

I think of this as โ€œHBO is Sex from Head to Toeโ€: HBO shows have a lot of nudity and what not, the sex helps me think of HbO + seX = HOX; it's for arrangement from the head to the toe.

One of the cervical has become a thoracic looking segment. So we have replaced a cranial segment (cervical) with something closer to the feet/ caudal (thoracic)

So the Hox gene at the top is expressing caudal info when it should be cranial at C7

get full access to all content โ‹… become a member
drdoom  essentially, this question is describing a situation where the โ€œorange genesโ€ got turned on in the yellow area +
drdoom  oh, it's not that โ€the Hox geneโ€ is expressing the wrong info, by the way; itโ€™s that the WRONG Hox gene is being expressed. This can happen when the wildtype Hox gene (cervical area) is mutated and so the thoracic Hox gene โ€œtakes overโ€ -- even though abnormalities happen, this mechanism protects the body from missing an entire segment (โ€œbetter to put the wrong thing there than nothing at all!โ€) +
an1  @drdoom how do we know this question was talking about HOX expressing the wrong info vs HOX being wrong itself? Since all the other segments are assumed to be normal. wouldn't they be affected too if HOX was wrong all around? +
drdoom  Because HOX genes encode transcription factors. Each HOX transcription factor, in turn, governs many other genes (turns on some, represses others) which direct development of a segment. Itโ€™s unlikely a single mutation in a HOX gene โ€œflipsโ€ it from directing cervical development to directing thoracic development. It's more likely that cervical HOX tf became dysfunctional (โ€œLoss of Functionโ€ mutation), which results in thoracic HOX tf to โ€œtake overโ€. +1
drdoom  Oh, I should have mentioned: each HOX box is a different/separate gene. It's not all one gene. It's a family of genes so a mutation in one will be independent of the others. +

 +2  visit this page (nbme18#21)
get full access to all content โ‹… become a member

Common Chelators:

  • Iron
  • Calcium
  • Mg
  • Aluminium

Commonly Chelated Drugs:

  • Tetracyclines
  • Fluoroquinolones
  • Levothyroxine

These create insoluble complexes and are inhibited from being absorbed!

get full access to all content โ‹… become a member
an1  ^Best way to avoid is to take meds at different times in the day +

 +0  visit this page (nbme18#29)
get full access to all content โ‹… become a member

The cavernous sinus contains CN 3,4,V1,V2, and 6 (right next to the ICA).

A: MCA defect (face and upper limb)

B: olfactory (recall that this is the only sense spared in thalamic strokes)

C: damage to macula, could be an MCA defect?

D: MCA; supplies parental and temporal(total HH, macula NOT spared), PCA; supplies occipital and some of temporal (total HH, macula spared) - mentioned pareital and temporal because of the quadrantonopis; 2 quads = 1 hemianopsia

E: LR (recall LR6, SO4)

get full access to all content โ‹… become a member

 +1  visit this page (nbme18#36)
get full access to all content โ‹… become a member

Correct me if I'm wrong. But I think both types of Pneumocytes sit in the basement membrane. Damage to Type 2 results in an inability to restore lung tissue (they regenerate 1 and increase surfactant) whereas type 1 is used for gas diffusion. So if the BM with the type 2 pneumocystis is damaged, no restoration. I didn't pay much attention to preclude though lol...

get full access to all content โ‹… become a member

 +0  visit this page (nbme18#17)
get full access to all content โ‹… become a member

21-OH is the most common def, and it has 3 subtypes.

1) A Classic salt wasting: at birth, dehydrated, low Aldosterone (high K, low H, low water), ambiguous genitalia

2) A classic non salt wasting: at birth, ambiguous genitalia, fluid level normal

3) non classic late subtype which is basically A/S and just has girls with acne, oligomenorrhea and hirsutism.

High 17 indicates that the defect must be 21.

11 defects --> 21 will be high because 11 comes after 21, hypertension will be seen

watch Dr. Randy Neils YouTube video on this, amazing job!

get full access to all content โ‹… become a member

 +2  visit this page (nbme18#45)
get full access to all content โ‹… become a member

Kaposi Sarcoma --> up regulation of VEGF --> treat with an anti-VEGF eg. bevacizumab (anti-neoplastic)

get full access to all content โ‹… become a member

 +2  visit this page (nbme18#7)
get full access to all content โ‹… become a member

The kidney on the right side lies slightly lower because the liver pushes it down. So the border is sort of rib #11.5 or 12th between the liver and the right kidney.

On the left side, the border between the spleen and the left kidney is the 11th rib --> 9th and 10th are above this so the injury was to the spleen. Also recall that the MOST commonly damaged organ after trauma is the spleen.

get full access to all content โ‹… become a member

 +1  visit this page (nbme18#43)
get full access to all content โ‹… become a member

Like another common stated, B,C,D,E are wrong right off the bat. A says DISCUSS treatment and referral. It's not the same as saying refer to etc. Even if referral threw you off, don't you think it's important to ask the patient why he's doing what he is and if he wants to change/ or know the long term effects rather than straight up saying "here, take some methadone. it'll help you quit". what would you want in this patients shoes? someone to help you through the situation step by step (most probabaly)

get full access to all content โ‹… become a member

 +2  visit this page (nbme18#31)
get full access to all content โ‹… become a member

โ†‘Blood solubility: slow speed

โ†“Blood solubility: fast speed

โ†‘Lipid solubility: very potent

โ†“Lipid solubility: not potent

Potency = 1/ MAC

get full access to all content โ‹… become a member

 +0  visit this page (nbme18#31)
get full access to all content โ‹… become a member

Important to not confuse the equations on this one. Because they asked for women only, we can eliminate the mens information.

RR = ET/ EC =33%

ARR = EC - ET = 8%

RRR = EC - ET / EC = 67% (our answer)

get full access to all content โ‹… become a member

 +2  visit this page (nbme18#47)
get full access to all content โ‹… become a member

Holosystolic: MR, TR, or VSD

Lower left sternal border (the left border is Erb's point, beneath that is the Tricuspid area) --> TR or VSD

Whats more common? VSD (by far!!)

If they had mentioned the mum having BPD or taking pills for a psych disorder, then TR could be a big contender.

get full access to all content โ‹… become a member

 +0  visit this page (nbme18#31)
get full access to all content โ‹… become a member

so this patient had a very tender thyroid gland.

first start ruling out. no exop was trying to say its not graves. she also had a LOW TSH (indicating it was hyperthyroid ~ recall that many hypothyroid conditions present with primary hyperthyroidism labs).

there wasn't enough to support A here (should have low iodine uptake and low thyroglobulin).

thyroid abscess needed a fever and is just an odd Dx.

Toxic MNG and subacute left.

subacute or de quervains is VERY painful. if you look in the endo section, subacute is actually the ONLY tender condition

get full access to all content โ‹… become a member

 +1  visit this page (nbme18#13)
get full access to all content โ‹… become a member

Concentric: in order of most to least common

1) HTN

2) Aortic Stenosis

3) HCOM

Concentric is a Chunky wall (the ventricle is not dilated, on the wall is thicker)

get full access to all content โ‹… become a member
claves  FA 2020 pg 308 +

 +0  visit this page (nbme24#19)
get full access to all content โ‹… become a member

C,D and E were obviously wrong. A and B were left. I opted for B, but then changed it. A nurse may not be able to catch the same things a doctor could. And also, A says to ASK. She has the right to say no, and what happens after that is of no concern to us in this scenario. Theres never any harm in asking.

get full access to all content โ‹… become a member
madamestep  Yeah I went with the default of discussing furhter +

 +1  visit this page (nbme24#34)
get full access to all content โ‹… become a member

I use parasympathetic/ sympathetic principles to figure this out. If you're laying down, you're most likely resting and digesting. That rules out E, C (RAAS is due to high Sympathetic tone) and also D (high plasma volume is a result of RAAS). This left A and B. Decreased plasma sodium volume would have been the case if he was drinking a lot of water, or had SIADH possibly. I couldn't really find the connection between this option and his PNS activity. So I went for A, especially because it was directly opposite of one option I KNEW was wrong.

get full access to all content โ‹… become a member

 +0  visit this page (nbme24#6)
get full access to all content โ‹… become a member

High Alkaline phosphates (bone, GB, liver)--> test the GGT

High GGT indicates gall bladder issue (ALKP >> AST & ALT)

Low GGT is liver disease (ALKP << AST & ALT)

Bilirubin is high in both

Unconjugated is high when there's a def of UDP-glucoronylase. This guy has stones in the CBD; they can't get out. that's going to be increased conjugated bilirubin

get full access to all content โ‹… become a member

 +0  visit this page (nbme24#18)
get full access to all content โ‹… become a member

I feel like everyone is talking about all these reactions when I just draw out the graph. We wanted to increase the Km (move it on the X axis), that would lead to it crossing on the y axis (Vmax). if we kept the Km at the same spot, it wouldn't overlap the point on the max else they'd have been the exact same lines...

get full access to all content โ‹… become a member
an1  ^^ if we kept the Km at the same point, it wouldn't overlap the point on the Vmax and if it did, they'd have the same lines** +

 +2  visit this page (nbme24#1)
get full access to all content โ‹… become a member

NADPH def: CGD --> infections with catalase + (SNAPS - staph species, nocardia (NOT actinomyces), aspergillus, pseudomonas (esp cepacia), serrate marcescens) ~ Dihydrorhodamine or nitroblue tetrazolium testing MPO def: candida infections, responsible fro green colour of sputum

get full access to all content โ‹… become a member

 +0  visit this page (nbme24#37)
get full access to all content โ‹… become a member

UW: "gaps between endothelial cells allow blisters to form". this guy has a blister.

get full access to all content โ‹… become a member

 +1  visit this page (nbme24#1)
get full access to all content โ‹… become a member

Was about to choose decreased transferrin because I couldn't see hyper-segmented neutrophils. But NBME often tries to throw us off with vague images. So I read again. Caught the "Ileal resection". Iron Fist Bro! Ileum is B12 absorption. B12 results in megaloblastic anemia. N5-MTHF is a step in converting DHF into THF. Inhibited in megaloblastic anemia like B12 and B9 def.

get full access to all content โ‹… become a member
an1  Also recall, that B12 is stored for many years. so presenting with a def years later (I agree 10 is a jump but still) is an indicator too +

 +0  visit this page (nbme24#13)
get full access to all content โ‹… become a member

"splinting" (pushing the vaginal canal with fingers to defecate) is commonly seen with a rectocele.

+Pelvic organ prolapse includes pelvic pressure ("feeling a bulge or that something is falling out of the vagina")

+Posterior vaginal wall prolapse (rectocele) can cause constipation

+splinting is common but not uterine enlargement

+Premenopausal, nonobese nulliparous women are at lowest risk for pelvic organ prolapse.

https://www.pelvicexercises.com.au/wp-content/uploads/2019/05/Rectocele-prolapse-min.png

Stool seems to go towards the vaginal wall, but doesn't come out. pushing the POSTERIOR vaginal wall towards the bum will help with defecation

get full access to all content โ‹… become a member
drdoom  quick tip! if you want to make a bulleted list, put a space after the โ€™+โ€™ sign ๐Ÿ‘ +1
an1  I tried haha, this is what came out lol +
drdoom  there is no space after your plus sign above; if you put a space after, it will work! (``+ Pelvic`` instead of ``+Pelvic``) hope that makes sense! +1

 +0  visit this page (nbme24#7)
get full access to all content โ‹… become a member

Asking about the CAUSE, not the response. The cause for a dilated ureter is increased GFR.

4 values are considered Pc (increases push into ureter direction) Pi (increases push into bowmans) ฯ€c (increases pull into bowmans) ฯ€i (increases pull into direction of ureter)

If ureter is dilated, the bowmans capsule is PUSHING out more fluid โ€”> increased GFR (high Pc) and pulling less (low ฯ€c)

Got this wrong because I thought they wanted to know what the response would be...

get full access to all content โ‹… become a member
an1  to add to comment ^: B, C, D donโ€™t affect GFR. E would increase GFR but is unlikely to be the cause here. +

 +0  visit this page (nbme24#37)
get full access to all content โ‹… become a member

Goljian: Pregnancy/ OCP use: High T4, normal TSH Steroids(anabolic): Low T4, normal TSH

get full access to all content โ‹… become a member

 +0  visit this page (nbme23#16)
get full access to all content โ‹… become a member

Resistant to digestion: does not break or get deactivated (endonuclease creates a nick in the strand, which means that it BREAKS the strand; even if it is for correction purposes) Deactivation is done by methylation; so if methylase is defective, the sequence will never be muted (digested/ broken down/ cleaved)

get full access to all content โ‹… become a member
an1  This could have also been written as deacetylation^^ +

 +1  visit this page (nbme20#36)
get full access to all content โ‹… become a member

the child was in a daycare, sonnei and rotavirus are the ones to keep in mind. sonnei can also be due to unwashed veggies too. and the inflammatory stool (neutrophils) also indicates sonnei. the lack of exposure (undercooked meat for EHEC) helps to rule out E.Coli. dirty water (ETEC and EIEC) aren't possible because of this kids bloody stool. Also for this to be HUS (the only possible E.Coli with bloody diarrhea), we should have seen the triad or at least something about it (anemia + thrombocytpoenia + Acute Renal Insuff.). Also, "mucoid stools" is right from the FA chart for shigella.

get full access to all content โ‹… become a member

 +0  visit this page (nbme20#30)
get full access to all content โ‹… become a member

I just used common sense to rune out the answers here. Firstly, knowing that cortisol is increased during times of stress (starvation; like this stem). Insulin causes hypoglycaemia so the body wouldn't produce more in a stressful state (expect glycogen to be higher). IGF-1 acts like GH and these states of growth require energy which this man clearly doesn't have. There wasn't enough to support testosterone and T3 changes so those were ruled out pretty quick.

get full access to all content โ‹… become a member

 +2  visit this page (nbme16#3)
get full access to all content โ‹… become a member

I had this narrowed down to Influenza virus and 23-Valnet Pnuemococcal. I was opting fro 23 but this patient actually has a dry cough, whereas Strep P often has a productive, rust coloured cough. Also, Strep Pneumo often causes pulmonary consolidation and so breath sounds would be increased. But don't forget, influenza can increase the risk of staph aureus pnuemo!

get full access to all content โ‹… become a member




Subcomments ...

submitted by an1(114), visit this page
get full access to all content โ‹… become a member

Common Chelators:

  • Iron
  • Calcium
  • Mg
  • Aluminium

Commonly Chelated Drugs:

  • Tetracyclines
  • Fluoroquinolones
  • Levothyroxine

These create insoluble complexes and are inhibited from being absorbed!

get full access to all content โ‹… become a member
an1  ^Best way to avoid is to take meds at different times in the day +


submitted by nwinkelmann(366), visit this page
get full access to all content โ‹… become a member

FA 2019 page 308. Most common cause of acute/primary pericarditis is assumed to be viral.

get full access to all content โ‹… become a member
cbreland  Primary made me think that it couldn't be acquired from virus/bug +6
an1  viral OR idiopathic* +
fhegedus  FA 2020 page 313 +


submitted by solidshake(25), visit this page
get full access to all content โ‹… become a member

Acute stress disorder involves flashbacks of traumatic event, avoidance of triggers, depressed mood, and nightmares; lasts 3 days - 1 month; can evolve to PTSD if lasts >1 month

Panic Disorder is recurrent and happens unexpectedly without known triggers

Biploar and Histrionic easily ruled out

Alcohol Withdrawal is left as the right answer. Symptoms also match with time course. Delirium tremens 2-4 days after last drink

get full access to all content โ‹… become a member
an1  Totally agree with you. But I don't think she's having DT just yet. It's been 2 days (48 hours) so we can expect to see Alcoholic Hallucinosis, which explains the vague shapes she's seeing. +1


submitted by t123(32), visit this page
get full access to all content โ‹… become a member

This question is really testing what the different types of diarrhea show. Key is "stool shows no abnormalities". In malabsorption, exudative, osmotic, and secretory diarrhea, your poop would be weird in some way. A motility disorder is the ONLY type here that would cause normal poop.

get full access to all content โ‹… become a member
myoclonictonicbionic  How would stool be different in secretory or osmotic diarrhea? They state that he has loose stool which could also indicate osmotic/secretory diarrhea. I think they are trying to hint that he has diabetes for 26yrs therefore he has diabetes enteropathy and therefore motility issues +6
takayasuarteritis  I'm with you on this. I think it's a myenteric nerve plexus issue from long-standing diabetes. +14
drpee  Neuropathy makes sense for T1DM, I guess I just expected a motility issue to cause constipation rather than diarrhea... +19
mnunez187  Moving too fast or moving too slow +
an1  @drpee yeah same, UW mentioned that damage to enteric nerves in DM leads to constipation, so I thought the motility disorder should have constipation +


submitted by match95(56), visit this page
get full access to all content โ‹… become a member

Transposition of the vanA gene from vancomycin-resistant Enterococcus is how it transfers resistance. They use transposons which are located on plasmids. If you have plasmid loss, you won't have transposons, and resistance will decrease.

get full access to all content โ‹… become a member
azibird  Why can't this be a point mutation? +6
freenbme23  I don't think that this implies that it can't be point mutation, but rather plasmid loss is more likely. Also, the point mutation Would have to ultimately lead to the plasmid loss. +
thrawn  FA says transposition is responsible for antibiotic resistance and plasmids are for transferring the genes of toxins (though UW says also antibiotic resistance). Make up your minds sheeple +2
mariame  The most common Vancomicin resistant genes, vanA and vanB are found in a transposon. These have been transferred from Enterococcus to a multidrug resistance plasmid in Staph aureus. the super multidrug resistance plasmid now contains resistance genes against lactams, vancomycin, aminoglycosides, trimethoprim, and some desinfectants. +2
an1  @thrawn I recall that too, but I think it said transposition was antibiotic resistance and UW said transposons was for multi drug resistance +
uasid  The plasmid is lost during bacteria replication โ€“ when DNA is being replicated, the plasmid is not always replicated and passed on to subsequent generations, especially if there are several generations of replication. +1


submitted by jean_young2019(18), visit this page
get full access to all content โ‹… become a member

Could someone explain why this choice is the best answer? I struggled between A and D, and picked A finally, which is "ascertain educational level and provide publications".

get full access to all content โ‹… become a member
donttrustmyanswers  It isn't A, because research shows that understanding of information (i.e. eating good and exercising) isn't enough to cause change. Why it is Provide F/U, over support group, IDK. +6
thisshouldbefree  because it says "refer" and u never refer +2
an1  Reading publications is boring and may be beyond the scope of the patient. It's best to explain things in laymen terms and suggest articles if she shows interest @jean_young2019 +
epiglotitties  Random comment but I'm curious, why are some comments pastel orange and others pinkish? What's the difference? +
drdoom  pink = specific question is being posed @epiglotitties +1


submitted by aakb(41), visit this page
get full access to all content โ‹… become a member

warfarin inhibits epoxide reductase which prevents gamma carboxylation of NEW vitamin K dependent clotting factors. the therapeutic efficacy of warfarin is delayed until prexisting/OLD factors get consumed, which usu takes at least 3 days.

Therefore, it will not affect the PT for at least three days because the old factors are still around. Since factor II has the longest half life, it takes the longest for the old factor II to go away/get used up and that is why the PT has not increased yet in this patient.

get full access to all content โ‹… become a member
mariame  I am confused, he has had already 2 days with Heparin, and Heparin enhances anti thrombin which inhibits thrombin. +2
an1  @mariame they're asking why the PT is normal. PT is in reference to warfarin more than it is to heparin (refer to PTT). The reason Heparin is given is because it'll have rapid effects, but long term we want to use warfarin. Protein C and S (Anti-coagulants) are lost first, but the coagulant factors already in the blood remain (7 goes first, 2 goes last). warfarin only affects formation of new factors, not ones already made +


submitted by an1(114), visit this page
get full access to all content โ‹… become a member

"splinting" (pushing the vaginal canal with fingers to defecate) is commonly seen with a rectocele.

+Pelvic organ prolapse includes pelvic pressure ("feeling a bulge or that something is falling out of the vagina")

+Posterior vaginal wall prolapse (rectocele) can cause constipation

+splinting is common but not uterine enlargement

+Premenopausal, nonobese nulliparous women are at lowest risk for pelvic organ prolapse.

https://www.pelvicexercises.com.au/wp-content/uploads/2019/05/Rectocele-prolapse-min.png

Stool seems to go towards the vaginal wall, but doesn't come out. pushing the POSTERIOR vaginal wall towards the bum will help with defecation

get full access to all content โ‹… become a member
drdoom  quick tip! if you want to make a bulleted list, put a space after the โ€™+โ€™ sign ๐Ÿ‘ +1
an1  I tried haha, this is what came out lol +
drdoom  there is no space after your plus sign above; if you put a space after, it will work! (``+ Pelvic`` instead of ``+Pelvic``) hope that makes sense! +1


submitted by an1(114), visit this page
get full access to all content โ‹… become a member

I feel like everyone is talking about all these reactions when I just draw out the graph. We wanted to increase the Km (move it on the X axis), that would lead to it crossing on the y axis (Vmax). if we kept the Km at the same spot, it wouldn't overlap the point on the max else they'd have been the exact same lines...

get full access to all content โ‹… become a member
an1  ^^ if we kept the Km at the same point, it wouldn't overlap the point on the Vmax and if it did, they'd have the same lines** +


submitted by an1(114), visit this page
get full access to all content โ‹… become a member

Was about to choose decreased transferrin because I couldn't see hyper-segmented neutrophils. But NBME often tries to throw us off with vague images. So I read again. Caught the "Ileal resection". Iron Fist Bro! Ileum is B12 absorption. B12 results in megaloblastic anemia. N5-MTHF is a step in converting DHF into THF. Inhibited in megaloblastic anemia like B12 and B9 def.

get full access to all content โ‹… become a member
an1  Also recall, that B12 is stored for many years. so presenting with a def years later (I agree 10 is a jump but still) is an indicator too +


submitted by drmohandes(193), visit this page
get full access to all content โ‹… become a member
  • SIADH โ†’ euvolemic hyponatremia โ†’ normotensive / hypertensive
  • ACTH increases cortisol โ†’ hypertension (alpha-1 upregulation & cortisol can bind to aldosteron receptors at high concentrations)
  • ACTH increases aldosterone โ†’ hypertension + hypokalemia (K+ dumped in collecting duct)

If patient -only- had hypertension: ACTH more likely than SIADH.

Patient with hypertension AND hypokalemia: 100% ACTH.

Don't feel bad friends, I also had this question wrong :(...

get full access to all content โ‹… become a member
rolubui  ACTH does NOT act directly on the zona glomerulosa to increase Aldosterone. ACTH acts only on the zona fasciculata to increase cholesterol and zona reticulata to increases sex hormones. +4
rolubui  NOT cholesterol I mean cortisol in zona glomerulosa +
jurrutia  Yes, but cortisol can act as a mineralocorticoid at when levels are super high. +
an1  @rolubui absolutely agreed! UW has a question where they ask about the precuor of aldosterone. I chose ACTH. WRONG they said, it's angiotensin 2. And yet these NBME writes are saying that ACTH is responsible for both cortisol and aldosterone? no. +


submitted by an1(114), visit this page
get full access to all content โ‹… become a member

Asking about the CAUSE, not the response. The cause for a dilated ureter is increased GFR.

4 values are considered Pc (increases push into ureter direction) Pi (increases push into bowmans) ฯ€c (increases pull into bowmans) ฯ€i (increases pull into direction of ureter)

If ureter is dilated, the bowmans capsule is PUSHING out more fluid โ€”> increased GFR (high Pc) and pulling less (low ฯ€c)

Got this wrong because I thought they wanted to know what the response would be...

get full access to all content โ‹… become a member
an1  to add to comment ^: B, C, D donโ€™t affect GFR. E would increase GFR but is unlikely to be the cause here. +


submitted by lsmarshall(465), visit this page
get full access to all content โ‹… become a member

"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.

get full access to all content โ‹… become a member
seagull  i'm pretty sure your a prof and not a student. +30
nor16  nevertheless, we are greatful for explanation! +1
niboonsh  I remember seeing a question describe parasternal lift in the context of pulm htn. still got this wrong tho fml +
anotherstudent  Did my question have a typo? It says O2 saturation in the right ventricle is 70, which is equal to the Right atrium and vena cava. It says the O2 saturation in the left ventricle is 82%, which is a decrease from the LA (95) but not equal to the RV, which is why I thought there wasn't a VSD, I assumed there was a weird shunt from the LV to some other part. Will O2 saturation not always equalize? +1
pseudomonalisa  This is a right to left VSD due to the pulmonic stenosis present in Tetralogy of Fallot. O2 sat will be low (70) in the right ventricle, and from there it'll enter the left ventricle and mix with freshly oxygenated blood coming from the left atrium (95). Because of the mixing, the O2 sat of blood in the left ventricle will be somewhere in the middle of 70 and 95 (82 in this case). You're correct, though, that most other VSDs are left to right and you'd see greater O2 sat in the right ventricle in that case (not sure if it equalizes with the left ventricle though). +1
furkan7  I does not need to equalizes.Moreover, in left to right shunt,left ventricle's O2 saturation is close to 100% +
an1  If the LV blood is going into the RV, why didn't it's O2 sat increase? neither did the pulmonary artery's. I agree it's TOF, but the sats really don't make sense for a VSD... +


submitted by lsmarshall(465), visit this page
get full access to all content โ‹… become a member

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.

get full access to all content โ‹… become a member
sympathetikey  Exactly. I knew it had to due with fusion of the neuropores but had never heard of sclerotomes. Thanks for the explanation. +17
hungrybox  Fuck I picked "Formation of neural tube" but yea that makes sense... that would affect the whole CNS +8
ruready4this  I also never heard of sclerotomes and I chose that and then switched it to formation of the neural tube because I thought that was close enough ugh close enough is not the right answer +2
ih8payingfordis  FA 2019 Pg 479. They don't specifically mention sclerotomes but you can review the different neural tube defects here :) +
failingnbme  everyone who selected neural tube is basically me :P +
an1  I knew it was fusion, but didn't know what sclerotomes were. so I went for the option with neural tube in it... FML. +


get full access to all content โ‹… become a member

How do you distinguish this from testicular torsion? Is it just because it started in the left flank?

get full access to all content โ‹… become a member
neels11  and there's no mass in the scrotum, whereas testicular torsion will have that "bag of worms" feel (along with a lack of cremaster reflex) testicular torsion usually happens in a younger age group +12
medpsychosis  @neels11 I would like to clarify a piece of information. I believe you are confusing Varicocele with Testicular Torsion. Varicocele will present with "bag of worms" feeling. While the absence of cremasteric reflex is a sign of testicular torsion. +22
johnson  This is the classic "loin to groin pain" of nephrolithiasis. +9
suckitnbme  Testicular torsion would also tend to have a unilateral high-riding testicle. +
an1  testicular torsion has high riding testis, that would have been a prevalent finding to push this towards TT +


submitted by kentuckyfan(47), visit this page
get full access to all content โ‹… become a member

Notice that A) Bronchoconstriction, B) Glandular secretion, D) Peristalsis, E) Vasodilation of skin are all under parasympathetic control.

The only sympathetic control is heart rate, which would increase.

get full access to all content โ‹… become a member
drzed  Vasodilation of the skin is under sympathetic control as well -- beta-2 receptors when stimulated cause vasodilation (via increase of cAMP in vascular smooth muscle). The key is recognizing that stimulation of a GANGLION of the pns will lead to release of NOREPINEPHRINE, which preferentially stimulates alpha-1 receptors. Those receptors will cause vasoconstriction. If the question asked what happens when you stimulate the adrenal medulla, the answer would be (potentially) vasodilation. This is because the adrenal medulla releases EPINEPHRINE which preferentially stimulates beta-1/2 receptors. +12
jesusisking  @drzed Awesome explanation except I think sympathetic response induces vasoconstriction in the skin though vasodilation in the muscles! +1
usmile1  @jesusisking yes you are correct! ฮฑ1: vasoconstriction in skin and intestine ; ฮฒ2: vasodilation in skeletal muscle (transmitter: only epinephrine!) +
an1  sympathetic response is going to fight or flight. you'll be sweating, you want the sweat to dissipate so your body temperature doesn't shoot up. To reduce temperature, there is vasoDILATION at the skin and vasoCONSTRICTION of the splanchnic vessels. Confirm with UW QID 19088 (image) +1
an1  ignore me^^ +
an1  actually no don't lol, check out the image it'll make sense. @drzed is correct, HR was a better option here though +
an1  re-read the question here. might be taking a big leap but maybe the electrical stimulation is a give away. Yeah stellate is SNS leading to HR increase, sweating, increased blood pressure but if it's electrical stimulation, why would the skin vasodilator? it vasodilator to get rid of excess heat, which shouldn't be present with a minor electrical stimulation +


submitted by kentuckyfan(47), visit this page
get full access to all content โ‹… become a member

Notice that A) Bronchoconstriction, B) Glandular secretion, D) Peristalsis, E) Vasodilation of skin are all under parasympathetic control.

The only sympathetic control is heart rate, which would increase.

get full access to all content โ‹… become a member
drzed  Vasodilation of the skin is under sympathetic control as well -- beta-2 receptors when stimulated cause vasodilation (via increase of cAMP in vascular smooth muscle). The key is recognizing that stimulation of a GANGLION of the pns will lead to release of NOREPINEPHRINE, which preferentially stimulates alpha-1 receptors. Those receptors will cause vasoconstriction. If the question asked what happens when you stimulate the adrenal medulla, the answer would be (potentially) vasodilation. This is because the adrenal medulla releases EPINEPHRINE which preferentially stimulates beta-1/2 receptors. +12
jesusisking  @drzed Awesome explanation except I think sympathetic response induces vasoconstriction in the skin though vasodilation in the muscles! +1
usmile1  @jesusisking yes you are correct! ฮฑ1: vasoconstriction in skin and intestine ; ฮฒ2: vasodilation in skeletal muscle (transmitter: only epinephrine!) +
an1  sympathetic response is going to fight or flight. you'll be sweating, you want the sweat to dissipate so your body temperature doesn't shoot up. To reduce temperature, there is vasoDILATION at the skin and vasoCONSTRICTION of the splanchnic vessels. Confirm with UW QID 19088 (image) +1
an1  ignore me^^ +
an1  actually no don't lol, check out the image it'll make sense. @drzed is correct, HR was a better option here though +
an1  re-read the question here. might be taking a big leap but maybe the electrical stimulation is a give away. Yeah stellate is SNS leading to HR increase, sweating, increased blood pressure but if it's electrical stimulation, why would the skin vasodilator? it vasodilator to get rid of excess heat, which shouldn't be present with a minor electrical stimulation +


submitted by sajaqua1(607), visit this page
get full access to all content โ‹… become a member

MHC I function is integral to cancer suppression. MHC I displays endogenously synthesized proteins and presents them to CD8+ T cells. The failure to display MHC I, or MHC I display of non-self (and by extension cancerous) proteins triggers a cellular immune response, leading to destruction of the cell.

The proteasome is used for the degradation of worn out, senescent, or malformed proteins. As cancer develops, more mutations lead to increased wrong proteins. Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I and lead to the cell being killed. Bortezomib blocks the proteasome, so the mutant proteins are displayed on the surface, allowing the immune system to recognize and kill pathological cells.

get full access to all content โ‹… become a member
catch-22  Another way to approach it is to think about MHC class I processing. Basically, if you inhibit the proteasome, peptides will not be generated and nothing is available to be loaded onto MHC I (remember MHC I has to be loaded before it's transported to the cell surface). Cells that don't express MHC I get killed by the natural killers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +32
kai  "In conclusion, we have demonstrated that the proteasome inhibitor bortezomib down-regulates class I and enhances the sensitivity of myeloma to NK cellโ€“mediated lysis" from the conclusion of the NIH paper +6
maddy1994  another mechanism is by blocking proteosome u even decrease degration of proapoptotic proteins...so it enchances apoptosis(from uworld) +6
azibird  But CD8+ and NK cells kill via perforin! Why is this answer wrong? Is it because it's not the primary effect? +2
testready  "The proteasome is the major source of proteolytic activity involved in the generation of peptides for presentation by major histocompatibility complex class I molecules. We report the new observation that bortezomib down-regulates HLA class I on MM cells, resulting in increased NK cellโ€“mediated lysis." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +
fatboyslim  I think what OP said contradicts with what @catch-22 cited in the PubMed article. +
an1  OP said "Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I". UW QID 11674 says that a protein undergoes degradation by the ubiquitin proteasome pathway, after which it goes to the ER and then is presented to the cell surface for MHC 1 response leading to apoptosis via performs and granzymes. Having a proteasome inhibitor would actually prevent the MHC response because no proteins are displayed. Also note that the question says which process will be affected, there is no mention of increase or decrease. So yes, the MHC 1/ CD8 pathways is affected, but it's actually down regulated. An absence of MHC 1 leads to NK cell mediated death. +


submitted by usmleboy(19), visit this page
get full access to all content โ‹… become a member

Could someone explain why "Cardiac catheterization with stent placement" is incorrect?

My thought process was that this guy has an occlusion of his RCA --> knocking out his AV node --> 3rd degree AV block. Also his pulse is 40 which suggest a RCA infarction as well.

The reason I went with this is because he got to the hospital within 30 minutes and they put this information first and made it seem important. If his RCA could be opened up, then the damage could be reversible.

I get the pacemaker, but first I feel like you would attempt to unocclude the vessel and give it some integrity.

get full access to all content โ‹… become a member
hajdusa  That choice is incorrect because you can't assume that he has an occlusion from the information that you have. There can be many etiologies of a heart block, and they do not have to be ischemic in nature - for example there are different microbes that can cause heart block too. Additionally, if this guy were to have an RCA occlusion you'd likely see evidence of ischemia or infarction on the ECG but the only findings we're given are bradycardia and 3rd degree block. Hope this helps! +2
mtkilimanjaro  Also, the two cardiac catherization options would ultimately result in a similar outcome. It's like how the poster above mentioned the two imaging are very similar that you can rule them out. +
an1  AV block treatment is with a pacemaker. Straight from FA. The only time you'd want to do stenting is when there is stenosis (>70%) leading to angina, or an MI. Those could be potential differentials here but they flat out said he had an AV block so it's not the best approach. Also, the RCA supplies the SA node, the PDA supplies the AV node. AV block is due to AV node, Sick sinus syndrome would be due to SA node (dropped P wave rather than QRS. +1


submitted by armymed88(49), visit this page
get full access to all content โ‹… become a member

Glucose is co-transported into enterocytes of SI via sodium

get full access to all content โ‹… become a member
toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +4
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +4
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +2
makinallkindzofgainz  *dehydrated +
teepot123  salt and sugar, that's all the kid needs when ill simple +1
mtkilimanjaro  Hm I put bicarb/K+ since thats lost in diarrhea, but I think the key thing in this Q is that its only 6 hours of acute diarrhea and nothing else. You would prob give bicarb and K+ in more "chronic" diarrhea over a few days or longer not just a few hours +1
specialist_jello  ugh i overthought the question and changed my answer to bicarb/k +
an1  SGLT1 in the gut is a symporter. Glucose is needed to allow Na to enter, water will follow Na into the cell and reduce dehydration. Be sure to give a HYPOtonic ORS solution (more water than salt and sugar), otherwise solutes (move from low to high OSm will leave the tissues and enter the vasculature. +


submitted by usmlehulk(7), visit this page
get full access to all content โ‹… become a member

can anyone please explain why option E which is increased in Urinary pH is not the correct answer. becasue hydrogen wasting is also a form of correcting respiratory acidosis.

get full access to all content โ‹… become a member
wfma888  right- you will increase excretion of protons which will LOWER the pH! +2
an1  โ†‘ urine excretion of HCO3 (represents the alkaline pH/ higher pH) and โ†‘ urine pH are the same thing. Yes, you may wonder now why the โ†‘ blood HCO3 didn't cause an alkalosis but that's because the PRIMARY effect was the retention of CO2 leading to decreased blood pH +
an1  HCO3 is alkaline compared to H is what I meant to say ^ +


submitted by usmlehulk(7), visit this page
get full access to all content โ‹… become a member

can anyone please explain why option E which is increased in Urinary pH is not the correct answer. becasue hydrogen wasting is also a form of correcting respiratory acidosis.

get full access to all content โ‹… become a member
wfma888  right- you will increase excretion of protons which will LOWER the pH! +2
an1  โ†‘ urine excretion of HCO3 (represents the alkaline pH/ higher pH) and โ†‘ urine pH are the same thing. Yes, you may wonder now why the โ†‘ blood HCO3 didn't cause an alkalosis but that's because the PRIMARY effect was the retention of CO2 leading to decreased blood pH +
an1  HCO3 is alkaline compared to H is what I meant to say ^ +


submitted by pg32(218), visit this page
get full access to all content โ‹… become a member

How did anyone get this as T cruzi? That was literally the first answer I ruled out. She has swelling of the eye, but that is the only sx that fits. Chagas presents 10-20 years after initial infection, not two weeks later. It also doesn't present with recurrent fever, muscle aches and joint pain. I mostly ruled it out because of the time course.

get full access to all content โ‹… become a member
castlblack  I made the same mistake. Tsetse flies only exist in africa. African sleeping sickness is named well. Chagas is only in south america/central. Leishmaniasis is found on both continents. +
medjay7  The clinical presentation confused as hell, but I could recognize that Trypomastigote anywhere and definitely was not African sleeping sickness. +2
usmleboy  She has the swelling of the eye, edema, and chest pain. T cruzi causes dilated cardiomyopathy (chest pain and edema), and the eye swelling (Romana sign) is pretty buzzwordy for Chagas. Also it looks like a trypanosome. +1
an1  -Acute: nonspecific S/S (fever, malaise, anorexia), inflammataion/ swelling at site of innoculation (chagoma), swelling around eye (Ramona) +


submitted by nwinkelmann(366), visit this page
get full access to all content โ‹… become a member

This article explains the pathophysiology well: https://www.ncbi.nlm.nih.gov/books/NBK431048/.

The right ventricle is primarily supplied by the RCA which also supplies the SA node and AV node (90% of hearts because they are right dominant), leading to loss of contractility of the right side, and thus fluid buildup causing elevated central venous pressure. Elevated pressures in the liver and portal system would lead to hepatomegaly and free fluid accumulation in the peritoneum.

get full access to all content โ‹… become a member
henoch280  Hellppp. pls why is it not decreased capillary oncotic pressure? +2
whoissaad  @ henoch280 Because there is no change in the levels of protein in the blood. +11
drzed  theoretically you could develop liver failure from the increase in central venous pressure (e.g. cardiac cirrhosis) and THEN you would develop a decrease in oncotic pressure. +2
an1  @henoch280 the patient had a RV failure. This means blood will start pooling backwards (raised JVP will be seen). But to answer your question, oncotic pressure changes when the albumin (protein) is low. This happens when the problem is with the liver, malnutrition, nephrotic/ nephritic leading to albuminuria. The heart results in a purely hydrostatic related defect. Hydrostatic means to PUSH fluid OUT of the vessels and into the tissues. This would results in fluid entering the systemic tissue (whole body edema is seen with RHF) and fluid entering into liver caused decreased drainage leading to ascites. Memorize pg 297 Capillary fluid exchange FA'2020 +1
l0ud_minority  @henoch280 also I think that increased pulmonary capillary hydrostatic pressure would explain a pleural effusion. I thought the same thing had to think about it for a bit. +


submitted by niboonsh(409), visit this page
get full access to all content โ‹… become a member

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

get full access to all content โ‹… become a member
ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please? +3
apurva  We usually look for c4d complement for humoral response in acute graft rejection. Because c4d makes covalent bond with the endothelium can can be found on staining because it is long lasting. +
an1  @ls3076 yep UW did say that. a humoral response is neutrophils, and a cellular is lymphocytic. that being said, lymphocytic is still the more likely out of the two by far. I recall this from a UW q, but don't rem the ID. Also, humoral usually takes weeks and cellular takes months. This kid was coming in 3 months post-op. +


submitted by tissue creep(133), visit this page
get full access to all content โ‹… become a member

Lifting head while prone: 1 month Social smile: 2 months Cooing: 2 months

get full access to all content โ‹… become a member
pg32  Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me +1
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +4
drzed  I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha. +9
snripper  Yeah, I don't see cooing anywhere. +
teepot123  thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol +1
pjpeleven  Mnemonic: "Coo at Two" +3


submitted by usmleuser007(464), visit this page
get full access to all content โ‹… become a member

my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
get full access to all content โ‹… become a member
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work +2
mcl  I love this and I love you +10
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested +3
leaf_house  @uslmeuser007 "MAMML PONNK" is the best I can do with that +1
an1  FLOCK MAMa (neuroFibromatosis 1 + 2, Leimyoma, Osteosarcoma, Cardiac angiosarcoma, Kaposi, Medullary Thyroid, Anaplastic Thyroid, Meningioma) +1
l0ud_minority  Also Buzz word for Kaposi's sarcoma is SPINDLE +


submitted by xxabi(293), visit this page
get full access to all content โ‹… become a member

Bronchogenic carcinoma = lung cancer

That being said, lung adenocarcinoma specifically is associated with hypertrophic osteoarthropathy, which is a paraneoplastic syndrome characterized by ๏ปฟdigital clubbing, arthralgia, joint effusions, and periostosis of tubular bones

get full access to all content โ‹… become a member
luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +2
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +8
yotsubato  This is in FA 2019 page 229 +11
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +5
waterloo  the clubbing is the symptom that takes out alot of the answer choices. It's super tricky. +
jawnmeechell  Plus the patient has an 84 pack-year smoking history, super high risk for lung cancer +
veryhungrycaterpillar  FA 2019 pg 229 is all paraneoplastic syndromes. There is no mention of bronchogenic carcinoma in any of them. There is adenocarcinoma, but that is most likely in non smokers, not in someone with 84 pack year of smoking history. Why does he have 5 upvotes for referencing first aid here, what am I missing? +3
jakeisawake  @veryhungrycaterpillar sounds like bronchogenic carcinoma is a general term for lung cancer. You are right that if a non-smoker gets lung cancer it is most likely adenocarcinoma as non-smokers rarely get small cell. However, smokers can get adenocarcinomas as well. The oncologist that I shadow sees this frequently. Adenocarcinoma of the lung causes hypertrophic osteoarthropathy per 229 in FA2019 +2
mangotango  @verhungrycaterpillar @jakeisawake Adenocarcinoma is the most common tumor in nonsmokers and in female smokers (like this patient), so adenocarcinoma would still be the most likely cancer for this pt over the others. Pathoma Pg. 96. +3
fatboyslim  Apparently bronchogenic carcinoma is basically an umbrella term for lung cancer. Source: https://radiopaedia.org/articles/lung-cancer-3 +
lifeisruff  bronchogenic is another term for adenocarcinoma in situ according to pathoma +1
topgunber  With the exception of mesothelioma- 95% are bronchogenic +1
meja2  @lifeisruff No, bronchogenic carcinoma is a blanket term for all lung cancers. However, the adenocarcinoma in situ subtype is called Brochoalveolar ca. Ref: FA 2018, pg 665. +1
an1  She also has a few symptoms to support it (cough, sputum, smoker). The swelling may throw you off and seem like RA but her age doesn't really fit the disease (also, no plastic lesions). New bone formation is a give away. UW says that bone forming cancers are prostate, Hodgkin and small cell whereas lytic are non-hodgkin, non-small cell, renal. GI and melanoma fall in between the blastic/ lytic spectrum. Clubbing is another give away (seen in lung CA, TB, CF, empyema, bronchiectasis, chronic lung abscesses, cardiac cyanotic diseases, infective endocarditis, IBD, hyperthyroidism, and malabsorption. a) young males with bamboo spine and sacral pain c) presented earlier (cyanotic diseases present in babies and need early correction) d) look for some HSM and jaundice related findings or maybe a history of infection routes e) honeycomb appearance, clubbing is present but not often related to bone findings g) often presents with CREST (limited), or skin (diffuse), antibodies + +1
an1  correction: GI and breast are mixed, melanoma is lytic as is multiple myeloma +


submitted by aoa05(34), visit this page
get full access to all content โ‹… become a member

Weakness with decreased muscle bulk implies problems that include the lower motor neuron system. Decreased DTRs implies a disrupted reflex loop but the absence of sensory loss implies that it is on the motor side of the reflex loop. Of the available choices, B is the best fit. "A" is arguably true because a strictly motor polyneuropathy (such as in lead poisoning) could account for the findings, but a 3-month course could hardly be called "acute."

get full access to all content โ‹… become a member
itsalwayslupus  I was able to deduce the right answer, but what is the specific reason against "demyelination of the corticospinal pathways"? just out of curiousity +1
lsp1992  I believe it's because damage to the corticospinal tract would be considered UMN damage, while degeneration of motorneurons is LMN damage. LMN damage causes decreased reflexes. UMN disease would cause hyperreflexia....I think. That's how I reasoned through it at least +20
nbmeanswersownersucks  I also think you can rule out peripheral neuropathy because typically that includes both motor and sensory +4
saqeer  yes but is not Achilles an S1 reflex (sacral cord) ? how does the degeneration in lumbar cord affects it ? i rule it out first thing because of this :S +
meryen13  i think she just had a dics herniation. there can be problem with temperature and sensation in some case but those are usually very severe herniations. not sure tho... but it can on your differentials. +
djeffs1  I assumed that "motoneurons of the lumbar chord" means upper and not peripheral +
sexymexican888  Is this ALS? +1
dawgtor  @saqeer , i had the exact same question. Can someone please help me out with this? +
ali_hassan  well pateller reflex is also diminished and it's an L3/L4 reflex so I wouldn't have ruled it out that quickly. I agree with @meryen13 it was probably a disc herniation that affected L and S of the spinal cord +
chaosawaits  How would "loss of afferent Ia axons innervating muscle spindles" present? That's the other I was torn between. +2
an1  @ sexymexican888 seems like it, but ALS is LMNL + UMNL. this patient only has LMNL. UMNL is a neuron issue before decoration, whereas LMNL will be affecting regions after the decussate (as in when they've reached the spinal cord) +


submitted by bingcentipede(359), visit this page
get full access to all content โ‹… become a member

This is hereditary spherocytosis. The image stinks, but the cells are not super pale in the middle and they're round. Her dad also had a splenectomy (HS is autosomal dominant), which is the definitive treatment for HS.

Pt is also normocytic (90.2 um^3), so a lot of the other answer choices can be eliminated based off this.

In the end, screw this picture because it's not clear and you can't zoom in.

get full access to all content โ‹… become a member
motherhen  Sad picture... I definitely thought this was B-thalessemia since the image looked like different size and shaped RBCs (anisopoikilocytosis). But if I squint my eyes real hard and turn sideways I guess I can also see those spheres +4
furqanka  beta thal, iron def and inadequate epo would have low reticulocyte count. impaired oxidative enzyme aka g6pd deficiency affects mostly males and would have bite cells +1
an1  Even if you can't see the picture, we can rule out B-thal, Fe def because these are microcytic. Oxidation defects are X-linked, so very rare to be seen in girls. adn that leaves EPO production. EPO production can be Relative (dehydration) or absolute (polycythemia where all the cells lines are increased and secondary; where there is hypoxia, high altitudes; no hx to support this or tutors like reninomb). we could deduce from the info given that its HS. but if all else failed, we can clearly see that we have some small and small 'larger' abcs. the small ones don' have colour variation. that makes HS the most likely +1


search for anything NEW!