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Comments ...

 +0  (nbme20#25)

So... theoretically an isolated decrease in HR would increase CO due to inc. preload, right?

But CO decreases in this case b/c the effect of inc. TPR is more powerful?

kernicterusthefrog  @hungrybox: No. Isolating HR, you would look at CO like this: CO=HR*SV so if HR or stroke volume go down, CO goes down. The change in preload wouldn't affect the CO as much as the change in rate of flow. So, the decrease in CO is solely due to the beta1 blocking effect on the AV node to decrease HR.

 +5  (nbme21#44)

other answers:

inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,

inhibition of phosphodiesterases (PDE):

  • theophylline (asthma) inhibits cAMP PDE
  • -nafils (dick pills) for ED inhibit cGMP PDE

β2 agonists: (for asthma) cause bronchodilation

  • albuterol (short acting - A for Acute)
  • salmeterol, formoterol (long acting - prophylaxis)

(idk lymphocyte membrane stabilization)

hungrybox  H2 blockers are the -tidines
yotsubato  > dickpills lol
temmy  hungrybox, you are a life saver
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2

 +3  (nbme21#24)

Macroscopically, squamous cell carcinoma tends to be off-white in color, arising from, and extending into a bronchus.

Source: Radiopedia

privatejoker  Lol am I the only one that picked Malignant Lymphoma? I thought I remembered Sattar mentioning that metastases are the most common form of cancer to be found in the lung? I tend to pick the "most common" presentation when given so little information to work with

 +14  (nbme21#17)

when diff single strand repair mechanisms are used:

  • repair newly synthesized strand: mismatch repair (Lynch syndrome)
  • repair pyrimidine dimers caused by dat UV exposure: nucleotide excision repair (Xeroderma pigmentosum)
  • repair spontaneous/toxic alteration: base excision repair
meningitis  Brca: recombinant repair

 +1  (nbme21#36)

enFUviritide -> used for fusion of HIV virus and target cell

aishu007  we can also say it enfuviritide blocks entry
aishu007  of virus into cell

 +5  (nbme21#25)

Relevant diagram

ATII constricts the efferent arteriole. ACE inhibitors block the ACE-mediated conversion of ATI to ATII.


eacv  here is a video for ilustration https://www.youtube.com/watch?v=US0vNoxsW-k

 +1  (nbme21#38)

My impression of Amphotericin B is that it's the BIG GUNS. It straight up attacks the sterols in the fungi plasma membrane.

Meanwhile lil bitch drugs like -azoles just inhibit sterol synthesis. (-terbinafine X lanosterol, -azoles X ergosterol)

Fungins X cell wall synthesis, flucytosine X nucleic acid synthesis.

et-tu-bromocriptine  Rule of thumb/shortcut: Nonserious fungal infections: treat with _conazole Serious fungal infection (eg, immunocompromised patients with disseminated infection): treat with amphotericin B Additional info The main classes of antifungal medications for usmle include: Polyenes (eg, amphotericin B, nystatin) - Bind to ergosterol molecules in fungal cell membranes, creating pores and causing cell lysis Triazoles (eg, _conazole) - Prevent the synthesis of ergosterol, a component of fungal cell membranes Echinocandins (eg, capsofungin, micafungin) - Inhibit the synthesis of glucan, a polysaccharide component of fungal cell walls Pyrimidines (eg, Flucytosine) - Converted to 5-fluoruracil, which then inhibits fungal RNA and protein synthesis
et-tu-bromocriptine  Ripppp the formatting, but hopefully the idea gets across
et-tu-bromocriptine  Fixed it, see comment!

 +14  (nbme21#49)

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks.
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox!
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."?

 +2  (nbme21#12)

Great video I used to learn this material.

  1. There are 3 major types of drugs: uppers (stimulants), downers (depressants), and hallucinogens.
  2. Heroin is an opioid. Opioids are downers.*
  3. Downers do what it sounds like. They cause "down" symptoms: sedation/decreased anxiety (and thus behavorial disinhibition), respiratory depression.
  4. Thus withdrawal will cause the opposite: hypertension/tachycardia, anxiety.
hungrybox  *other downers: alcohol, benzodiazepines, barbiturates
nwinkelmann  THANK YOU! for the link to the video. this is one thing I've ALWAYS struggled with.

 +2  (nbme21#1)

The cervix is the only structure that would result in bilateral blockade.

hungrybox  hydronephrosis = dilation of kidney (usu. due to obstruction at uretopelvic junction or backflow from obstructed bladder)

 +4  (nbme21#44)

Loop diuretics are first line for acute congestive heart failure. That should help you remember that they are the most potent diuretics, so they're often used in the acute treatment of edema.


 +5  (nbme21#41)

Loperamide: Agonist at u-opioid receptors. Slows gut motility (remember, constipation is a common side effect for all opioids).

quiz yourself:

Q: Would a junkie want to use Loperamide?

A: No, it has poor CNS penetration (which is why it has a low addictive potential).

Q: Would a junkie rather have morphine or buprenorphine?

A: Morphine. Both are u-opioid agonists, but morphine is a full agonist while buprenorphine is only a partial agonist.

Q: What about morphine vs. codeine?

A: Trick question, both are partial agonists.

cienfuegos  Thanks for passing off the knowledge. Regarding the last part, aren't morphine and codeine full agonists?
champagnesupernova3  Yes they are

 +1  (nbme21#18)

HIGH YIELD: "nonbilous vomiting" means that the issue/obstruction comes before (proximal to) the second duodenum, where bile is released.

At around ~4 weeks (give or take a few) is when pyloric stenosis usually shows up.

ez pts for u now keep it up


 +5  (nbme21#37)

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia.
mnemonia  Very nice!!
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei.
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla.
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps.
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are.
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion

 +3  (nbme21#50)

The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)

The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.

Source: Gray's Anatomy Review

hungrybox  Of note, the radial nerve innervates the extensors of the wrist. So the muscles of the anatomic snuffbox are all innervated by the radial nerve.
hungrybox  This helps you remember that the radial nerve innervates the abductor pollicis LONGUS (abductor pollicis BREVIS is median nerve, ADductor pollicis is the ulnar nerve. These two make sense if you think about the direction the thumb is moving - ending closer to the nerve.)


 +2  (nbme21#19)

aka ampulla of Vater or the hepatopancreatic duct

hungrybox  tripped me up cause I didn't know the names :(
sympathetikey  @hungrybox same
angelaq11  omg, same here! I thought, well, I don't know of any duct that connects the pancreas to the liver, so...2nd part of the duodenum it is :'( :'(

 +4  (nbme21#20)

quiz yourself answers:

  1. Sertoli (Sertoli Shuts down, MIF is secreted by Sertoli cells)
  2. 5-alpha reductase

 +10  (nbme21#20)

This video explains genital embryology extremely well.

If you felt totally lost like me, watch the video first at 2x, then check out the bottom figure on pg. 608 in FA 2019.

Relevant to this question:

  1. SRY proteins stimulate development of testes
  2. This pt has testes => he must have the SRY gene on the Y chromosome
  3. MIF degrades the Mullerian duct, which would otherwise become the internal female genitalia
  4. This pt has internal female genitalia => didn't make enough MIF

Quiz yourself (answers in a separate post):

  1. This patient's disorder can be traced back to which cells?
  2. This patient had normal genitalia. If this patient had smaller genitalia than normal, that would be a defect in what enzyme?
ergogenic22  I like to work backwards. 1) patient has normal testicles on histology, normal appearing penis this must mean a Y chromosome is present, as testis determining factor is on the y chromosome (see above post point #2). I.e. you can eliminate choice A and B. Theoretically, 47XY and 47XYY could also present with female genitalia due to lack of MIF, but normal 46XY is more common

 +2  (nbme21#26)

"cobblestone" appearance is associated with Crohn's disease

comparison of Crohn's vs UC



 +3  (nbme21#19)

jugular venous distention = left heart failure

pulmonary edema = right heart failure

Four-chamber dilation is the most likely answer.

Other answers:

  • Assymetric septal hypertrophy, myocardial disarray: these are both classic findings in hypertrophic cardiomyopathy (HCM)
  • endocardial fibroelastosis: a rare restrictive cardiomyopathy seen in infants/children
  • lymphocytic infiltration of the myocardium: seen in viral (autoimmune) myocarditis. A cause of dilated cardiomyopathy, but there was no mention of a preceding viral illness.
meningitis  I think you meant: Jugular venous distention = LT HF Pulmonary edema = RT HF
hungrybox  woops yea I meant Jugular venous distention = RIGHT HF, Pulmonary edema = LEFT HF

 -6  (nbme21#42)

preeclampsia presents differently:

  • symptoms: headache, blurred vision, abdominal pain, weight gain (water retention)
  • findings: hypertension, proteinuria, edema

 +7  (nbme21#3)

The 2 commandments of ethics questions:

  1. Don't ever pick an answer where you sound like a dick
  2. Don't ever consult the ethics committee

Served me well on this question.

linwanrun1357  If there is a choice about asking what the patient is worried about. Is this right? It does not sound like a dick :)
champagnesupernova3  If this were about a treatment asking why hes worried would be right but hes kind of doing the hospital a favor so I dont think you're supposed to try to convince or pressure him

 +5  (nbme21#23)

Huntington's disease

  • anticipation: she has a similar disorder as her father but died earlier

Remember "HUNT 4 an animal, put it in a CAGe". Huntingtin gene found on Chromosome 4. CAG is the trinucleotide repeat:

  • Chorea, caudate nucleus
  • Ataxia
  • Gloomy (depression)
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld.
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld.
foulari112  How would you differentiate this from Frontotemporal lobe dementia
temmy  Foulari 112..the ageof the patient and the anticipation cos her dad had it too. Also in frontotemporal pick, you will see personality changes where they act completely different vs huntington where they are aggressive and depressed.

 +4  (nbme21#8)

Wernicke-Korsakoff syndrome due to thiamine (B1) deficiency. Common in alcoholics.

The reason why they said "results of alcohol and drug screen are negative" is that the differential includes acute alcohol intoxication.

Wernicke's triad:

  • confusion
  • paralysis of eye muscles (ophthalmoplegia)*
  • ataxia

*presents here as nystagmus

Korsakoff's psychosis:

  • memory loss (anterograde and retrograde)
  • making shit up (confabulation)
  • personality change

 +5  (nbme21#11)

/u/cantaloupe5 had a great explanation.

Here's an image of the different stages following myocardial infarction. Note the "contraction bands" are what define coagulative necrosis.


 +10  (nbme21#15)

why hemolysis is wrong:

There should almost never be straight up bilirubin in the urine. In hemolysis, the excess bilirubin is excreted in the bile. After bacterial conversion and reuptake, some will be excreted in the urine as urobilin. However, in obstructive disorders, the conjugated bilirubin will never have the opportunity to undergo bacterial conversion to sterco/urobilin. In this way, the conjugated bilirubin has no other way to be excreted other than directly in the urine.

credits to /u/alacran763 on reddit


 +0  (nbme21#45)

According to the USMLE, selenium's only use is in selenium sulfide as a treatment for a fungus called Malassezia spp (Tinea versicolor).


 +7  (nbme21#20)

some wrong answers:

*makes sense b/c myeloblasts are precursors to granulocytes, which use MPO to fight off infections

temmy  Hungrybox aka life saver
hello  Thank you!!!

 -5  (nbme21#37)

Long answer ahead, but bear with me.

HINT: v looks kind of like y, whereas k looks more like x.

y-intercept = 1/Vmax

  • Vmax is the upper limit on how fast a reaction is catalyzed by enzymes.

x-intercept = 1/Km

  • Km is a ranking of how good an enzyme is at binding its substrate. An enzyme with a ranking of 1 is better at binding its substrate than an enzyme with a ranking of 5. (Lower Km = better enzyme)

Note that Vmax, as a measure of performance, can be altered through many things. Meanwhile, Km is a set characteristic of the enzyme, and cannot be altered.

In this example, the enzyme performance (Vmax) is increased by increasing the vitamin cofactor so that it reaches a "normal" activity. However, the enzyme is still inherently shitty due to a congenital defect, so the Km stays the same.

mnemonia  Awesome.
ht3  wait line B shows the vmax doesn't change and that the km is getting larger (enzyme is still shitty so larger km) so -1/km would be a smaller number and would approach 0
lamhtu  You say Km cannot be altered and its staying the same, but the answer of the graph demonstrates a higher Km value. Needing "higher concentrations" of the B6 for enzyme activity is another way of saying Km is higher since more is required for 1/2 vmax activity
sbryant6  Yeah this explanation is wrong.

 +6  (nbme21#1)

ethambutol = EYEthambutol

Great mnemonic for remembering that EYEthambutol is the component that causes visual problems in RIPE therapy for TB.

hungrybox  RIPE = rifampin, isoniazid, pyrazinamide, ethambutol

 +2  (nbme21#41)

other answers:

  • narcolepsy: Associated with hypnogogic or hypnopompic hallucinations.
  • hypnoGO to sleep = night time hallucinations

  • paroxysmal nocturnal dyspnea: PNH is a hemolytic anemia. No signs of hemolytic anemia (hematuria, jaundice, dec. haptoglobin).

  • sleep apnea: Associated with obesity, loud snoring.

doingit21  narrowed down to MDD and restless leg then convinced myself that elderly are at higher risk for MDD than RLS. Is that valid reasoning?
yb_26  Paroxysmal nocturnal dyspnea = breathless awakening from sleep, seen in left heart failure. It is not a paroxysmal nocturnal hemoglobinuria.

 +2  (nbme21#28)

Due to glycine's small size, it creates "kinks" in the amino acid sequence. These kinks are needed to correctly form the secondary structure.

Other answers:

  • "weakened interaction between collagen and proteoglycan" - collagen + proteoglycan = cartillage. The question stem mentions many defects in bONE (type I collagen) but no mention of defects in carTWOllage (type II collagen)

 +6  (nbme21#25)

Dysplastic nevi are a precursor to melanoma. They have irregular, "dysplastic" borders. Remember the "B" in ABCD stands for irregular Borders. Nevus means mole.

Other answers:

  • acanthosis nigricans - Darkening of skin associated with Type II diabetes mellitus

  • basal cell carcinoma of skin - Rarely, if ever metastasizes. Commonly affects upper lip.

  • blue nevus - Blue-colored type of common mole. Benign.

  • pigmented seborrheic keratosis - "Stuck on" appearance. Mostly benign. Affects older people.

  • (Note - you usually see only one. If multiple seborrheic keratoses are seen, it indicates a GI malignancy - aka "Leser-Trélat sign)
usmleuser007  correction ~ BCC affects the lower lip more than the upper
sympathetikey  Pathoma says upper lip, good sir
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin




Subcomments ...

submitted by hungrybox(241),

Dysplastic nevi are a precursor to melanoma. They have irregular, "dysplastic" borders. Remember the "B" in ABCD stands for irregular Borders. Nevus means mole.

Other answers:

  • acanthosis nigricans - Darkening of skin associated with Type II diabetes mellitus

  • basal cell carcinoma of skin - Rarely, if ever metastasizes. Commonly affects upper lip.

  • blue nevus - Blue-colored type of common mole. Benign.

  • pigmented seborrheic keratosis - "Stuck on" appearance. Mostly benign. Affects older people.

  • (Note - you usually see only one. If multiple seborrheic keratoses are seen, it indicates a GI malignancy - aka "Leser-Trélat sign)
usmleuser007  correction ~ BCC affects the lower lip more than the upper +  
sympathetikey  Pathoma says upper lip, good sir +6  
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin +2  


submitted by hungrybox(241),

jugular venous distention = left heart failure

pulmonary edema = right heart failure

Four-chamber dilation is the most likely answer.

Other answers:

  • Assymetric septal hypertrophy, myocardial disarray: these are both classic findings in hypertrophic cardiomyopathy (HCM)
  • endocardial fibroelastosis: a rare restrictive cardiomyopathy seen in infants/children
  • lymphocytic infiltration of the myocardium: seen in viral (autoimmune) myocarditis. A cause of dilated cardiomyopathy, but there was no mention of a preceding viral illness.
meningitis  I think you meant: Jugular venous distention = LT HF Pulmonary edema = RT HF +3  
hungrybox  woops yea I meant Jugular venous distention = RIGHT HF, Pulmonary edema = LEFT HF +3  


submitted by sympathetikey(316),

Direct Antiglobulin = Direct Coombs Test

Detects antibodies bound directly to RBCs. Hemolysis most likely due to something in the transfused blood (not sure why it took 4 weeks when Type 2 HS is supposed to be quicker but w/e).

ergogenic22  there is a delayed onset hemolytic transfusion reaction which should be evaluated with direct cooms test. https://www.ncbi.nlm.nih.gov/books/NBK448158/ +1  
hungrybox  such a dumb question wtf +8  


submitted by mcl(220),

Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.

hungrybox  Man this is such a nice figure except it doesn't have Krabbe disease :( +  
mcl  Here's another one with Krabbe! :) https://epomedicine.com/wp-content/uploads/2017/01/lysosomal-storage-diseases-enzyme-defects.jpg +4  
hungrybox  thank u +  
kjfhewiufh  [special] +  


submitted by jotajota94(9),

PDA flows from aorta to pulmonary artery decreasing afterload. Therefore cardiac output increases

seagull  doesnt pre-load also decrease which would drop the C.O.? +  
hungrybox  @seagull I think it would increase preload b/c more blood is going into the pulmonary arteries -> lungs -> pulmonary veins -> eventually more blood in left atrium/ventricle -> inc preload +4  


submitted by nuts4med(3),

Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?

haliburton  I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average. +1  
hungrybox  ty both of you for this, was wondering the same thing +  
coxsack  O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would). +2  
hungrybox  just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol) +1  
chandlerbas  ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter +  


submitted by kchakhabar(20),

This question is describing terminal insomnia, which is common either in MDD or normal aging. Out of those two MDD is the only thing in option choice. Plus, old age is a risk factor for MDD.

Even though the question does not describe 5 symptoms needed to diagnose MDD, MDD is the only logical choice.

hungrybox  excellent answer, thank you +2  


submitted by hungrybox(241),

other answers:

inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,

inhibition of phosphodiesterases (PDE):

  • theophylline (asthma) inhibits cAMP PDE
  • -nafils (dick pills) for ED inhibit cGMP PDE

β2 agonists: (for asthma) cause bronchodilation

  • albuterol (short acting - A for Acute)
  • salmeterol, formoterol (long acting - prophylaxis)

(idk lymphocyte membrane stabilization)

hungrybox  H2 blockers are the -tidines +1  
yotsubato  > dickpills lol +6  
temmy  hungrybox, you are a life saver +1  
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2 +  


submitted by mcl(220),

Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.

hungrybox  Man this is such a nice figure except it doesn't have Krabbe disease :( +  
mcl  Here's another one with Krabbe! :) https://epomedicine.com/wp-content/uploads/2017/01/lysosomal-storage-diseases-enzyme-defects.jpg +4  
hungrybox  thank u +  
kjfhewiufh  [special] +  


submitted by hungrybox(241),

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry +1  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +5  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +  


submitted by egghead(0),

This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.

hungrybox  same :( +  
masonkingcobra  My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp) [Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x) +  
gh889  FA 2019, pg 551 +3  
meningitis  Compulsively pulling out one’s own hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line; medications (eg, clomipramine) may be considered. +2  
step1soon  FA 2019 pg 551 +  


submitted by yo(26),

they're talking about a splenorenal shunt procedure

https://my.clevelandclinic.org/health/treatments/4950-distal-splenorenal-shunt

hungrybox  be honest did u know that before looking it up +2  
meningitis  @hungry, because you didn't know it, doesn't mean he didn't. This is a forum for answering questions and helping out, not dissing or showing off. Grow up before becoming a doctor. +1  
sympathetikey  Relax @meningitis. Hungry's just messin :) +1  
sbryant6  Looks like somebody needs an enema to get that stick out. +  
chandlerbas  ya'll are too TP/(TP+FN) lol +  


submitted by lnsetick(37),
  • APocrine = your armpits smell like an APE
  • ceRUMen = there’s no ROOM in your ears since they’re full of wax
  • EC-CRYne = when you ECercise, your pores are CRYing
  • SEBaceous = SEBum is SEEPing out of your pores
hungrybox  as an ape i'm offended +9  
dr.xx  stop being an ape. evolutionize! +5  
dbg  as a creationist i'm offended +  
maxillarythirdmolar  Also, Tarsal/Meibomian glands are found along the rims of the eyelid and produce meibum +  


submitted by hayayah(416),

Catheter placement:

https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg

Recall that the lung apex extends above the first rib.

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS +8  
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense. +4  
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization. +  


submitted by yo(26),

This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.

while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.

PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12

pneomina, right after all the infusion business and no mention of fever or anything? Nah.

go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.

Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.

hungrybox  we gonna make it bro +2  
hungrybox  or sis +2  
nala_ula  I did the same, basically went through each one and the time of onset between each. Good luck on your tests!! +  
temmy  i don't think pulmonary embolism will cause bilateral lung infiltrate +1  


submitted by yo(26),

This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.

while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.

PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12

pneomina, right after all the infusion business and no mention of fever or anything? Nah.

go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.

Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.

hungrybox  we gonna make it bro +2  
hungrybox  or sis +2  
nala_ula  I did the same, basically went through each one and the time of onset between each. Good luck on your tests!! +  
temmy  i don't think pulmonary embolism will cause bilateral lung infiltrate +1  


submitted by nosancuck(38),

hit me up wit dat HNPCC boi! all abou dat LYNCH SYNDROME

hungrybox  yee boi +  
mkreamy  hahahaha i fucking love both of you +  


submitted by yo(26),

under 8 years old for girls is a bad sign, 8 is okay. under 9 for boys is a bad sign.

just watch out for any 6 year old or something like that. beware of that GnRH either centrally or some some other source. -first aid 2019 pg 623

hungrybox  yo wtf i got my first dick hair in 6th grade wtf are they feeding these kids +8  


It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +8  
jcrll  "live-born offspring" ← baited +3  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +1  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  


submitted by nosancuck(38),

Bruh let me tell you a lil secret

PEEP prevents Atelectasis AKA dat LUNG COLLAPSE

Dont be worryin about random words they puts in front of the HIGH YIELD ones

hungrybox  literally LOL'd lmao I love this +1  


If anybody has a good way of distinguishing/remembering all the different presentations for genital sores, I'd appreciate the help.

hungrybox  Pls post as a separate post and not a comment to this tho. The formatting for these comments sux +  
whossayin  Assuming u have UWorld, just type sexually transmitted infections.. that table is the best IMO +  


submitted by neonem(263),

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

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +1  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +2  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +  
divya  absolutely right temmy. that's how i thought about it too. +  


submitted by hungrybox(241),

Great video I used to learn this material.

  1. There are 3 major types of drugs: uppers (stimulants), downers (depressants), and hallucinogens.
  2. Heroin is an opioid. Opioids are downers.*
  3. Downers do what it sounds like. They cause "down" symptoms: sedation/decreased anxiety (and thus behavorial disinhibition), respiratory depression.
  4. Thus withdrawal will cause the opposite: hypertension/tachycardia, anxiety.
hungrybox  *other downers: alcohol, benzodiazepines, barbiturates +  
nwinkelmann  THANK YOU! for the link to the video. this is one thing I've ALWAYS struggled with. +  


submitted by beeip(63),

This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

  • ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
  • The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation
jotajota94  Good job! Also, cortisol is involved in maintaining blood pressure. which was decreased in the patient. +3  
tinydoc  Decreased Na and increase K+ --- Hypoaldosteronisim Hypoglycemia, and hypotension --- Hypocortisolism so the adrenals arent working ---- adrenal Insufficiency the Hyperpigmentation comes from the increase ACTH as ACTH is from Proopiomelanocorticotropin. SO - increased ACTH also increases a -MSH ---> Hyper pigmentation. +5  
hungrybox  thank u for this answer +  
bilzcop  Ugh! I misread the question and chose ACTH :( +  
cienfuegos  @bilzcop: same +  
cienfuegos  @bilzcop: let's never do it again, k? +  
maxillarythirdmolar  Why does this patient have elevated BUN and creatinine?? +  


don't be a dick? not really sure what more there is to it. The patient doesn't have any other family so this woman should be considered family

aesalmon  Questions like this usually hinge on asking if you're going to follow the rules or not though, obviously the one asking her to lie and say she was her sister is wrong, but the correct answer is obviously breaking the hospice center's "policy" - presumably if the physician is sending her to hospice then they don't work there so why would the Dr. be able to just tell her its fine? +  
hungrybox  Yeah, I got this one wrong with the same logic as you, aesalmon. +  
emmy2k21  I genuinely interpreted this question as though the two women were in a relationship because of the quotes "my close friend". I figured significant others would be allowed to visit simply. Ha seems like I'm the only one who read too far in between the lines! +1  
dr_jan_itor  @emmy2k21 I also thought the quotes implied a lesbian relationship and that the patient was afraid to share this (they grew up at a time when it was heavily stigmatized). So i was thinking, of course you and your "special friend" can stay together. I know this is not just a phase +1  
et-tu-bromocriptine  Anything particularly wrong with A (Don't worry. I'll call you right away...")? It seemed like the most professional yet considerate answer choice. Are we supposed to imply that they're partners based on those quotation marks around "close friend"? Because otherwise it seems like too casual and less professional than A, almost as if it's breaking policy. +1  
lilmonkey  I can swear that I saw this exact same question in UWORLD before. The only reason I got it right this time. +  


submitted by hungrybox(241),

The cervix is the only structure that would result in bilateral blockade.

hungrybox  hydronephrosis = dilation of kidney (usu. due to obstruction at uretopelvic junction or backflow from obstructed bladder) +1  


submitted by hyoscyamine(21),

I know this is just a straight up fact from FA, but couldn't ureters (transitional cell carcinoma) also be correct?

hungrybox  Hmm I don't think so. The answer is "ureter" (singular) which would not result in bilateral hydronephrosis. +2  
privatejoker  If it is out of FA 2019, could someone give the page number to reference? Hydronephrosis' full definition is given on page 587 and makes no mention of invasive cervical carcinoma. +  
vinnbatmwen  p631 → Pap smear can detect cervical dysplasia before it progresses to invasive carcinoma. Diagnose via colposcopy and biopsy. Lateral invasion can block ureters - hydronephrosis - renal failure. +1  
privatejoker  Thanks! +  
emmy2k21  It's also in Pathoma page 140 in the 2018 edition! +  


submitted by cantaloupe5(37),

This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose? +5  
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then? +2  
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps. +1  
divya  sweet explanation imgdoc +  


submitted by hungrybox(241),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +1  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +1  


submitted by drdoom(211),

Vasoconstriction (narrowing of a tube) will cause the flow rate to increase through that tube, which decreases radial/outward pressure. The faster a fluid moves through a tube, the less “outward” force it exerts. (This is known as the Venturi effect.)

hungrybox  not seeing how this is relevant +1  
sympathetikey  He's showing how A & B are incorrect @hungrybox +1  


submitted by hungrybox(241),

The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)

The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.

Source: Gray's Anatomy Review

hungrybox  Of note, the radial nerve innervates the extensors of the wrist. So the muscles of the anatomic snuffbox are all innervated by the radial nerve. +  
hungrybox  This helps you remember that the radial nerve innervates the abductor pollicis LONGUS (abductor pollicis BREVIS is median nerve, ADductor pollicis is the ulnar nerve. These two make sense if you think about the direction the thumb is moving - ending closer to the nerve.) +  


submitted by hungrybox(241),

The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)

The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.

Source: Gray's Anatomy Review

hungrybox  Of note, the radial nerve innervates the extensors of the wrist. So the muscles of the anatomic snuffbox are all innervated by the radial nerve. +  
hungrybox  This helps you remember that the radial nerve innervates the abductor pollicis LONGUS (abductor pollicis BREVIS is median nerve, ADductor pollicis is the ulnar nerve. These two make sense if you think about the direction the thumb is moving - ending closer to the nerve.) +  


submitted by hungrybox(241),

aka ampulla of Vater or the hepatopancreatic duct

hungrybox  tripped me up cause I didn't know the names :( +5  
sympathetikey  @hungrybox same +2  
angelaq11  omg, same here! I thought, well, I don't know of any duct that connects the pancreas to the liver, so...2nd part of the duodenum it is :'( :'( +  


submitted by hayayah(416),

Note: The abducens n. is actually the nerve most likely to be damaged by an expanding internal carotid aneurysm in the cavernous sinus but they give you specific CN3 function in this question.

hungrybox  One pupil larger than the other indicates damage to the pupillary light reflex - afferent: CN II, efferent: CN III. +3  
cienfuegos  A little more info regarding other sxs (via UW): -cavernous carotid aneurysm: small usually asx, enlargement can cause u/l throbbing HA &/or CN deficits. VI most common thus ipsilateral lateral rectus weakness, can cause esotropia = inward eye deviation & horizontal diplopia worse when looking toward lesion -can also damage III, IV and V1/2 -can occasionally compress optic nerve or chiasm thus ipsilateral monoocular vision loss or non-specific visual acuity decrease +1  


Ok I get that if 500 already have the disease then the risk pool is dropped to 2000 students but the question specifically says that the test is done a year later...if 500 people had chlamydia, you would treat them. You don't become immune to chlamydia after infection so they would go back into the risk pool, meaning the pool would return to 2500. The answer should be 8%, this was a bad question.

thepacksurvives  Yeah, this was my issue. I got it wrong because of this-- still don't understand the logic bc you can get chlamydia multiple times +1  
hungrybox  FUCK you're right. Damn I didn't even think about that. That's fucking dumb. I guess this is why nobody gets perfect scores on this exam lol. Once you get smart enough, the errors in the questions start tripping you up. Lucky for me I'm lightyears behind that stage lmao +3  
usmile1  to make it even more poorly written, it says they are doing a screening program for FIRST YEAR women college students. So one year later, are they following this same group of students, or would they be screening the incoming first years? +3  
dashou19  I think the same at first, but after a second read, the question stem said "additional" 200 students, which means the first 500 students don't count. +  


submitted by nuts4med(3),

Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?

haliburton  I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average. +1  
hungrybox  ty both of you for this, was wondering the same thing +  
coxsack  O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would). +2  
hungrybox  just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol) +1  
chandlerbas  ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter +  


AV Fistulas re-rout blood from the arterial system to the venous system, by-passing the Arterioles = Increase PL ---> INCREASE VR. All in all = Increase CO.

According to UWorld, the arterioles are a major source of resistance ... so bypassing the arterioles results in a decrease in Total Peripheral Resistance ... causing an increase in the rate and volume of blood returning to the heart. I am pretty sure there is more to the physiology behind this, but I hope this explained a little.

big92  "Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554) There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH). +3  
hungrybox  Jesus big92 you went in on the research lmao u must be MSTP +2  
temmy  big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +  


submitted by seagull(437),

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD). +2  
hungrybox  To clarify - immature B cells have antibodies attached to their membrane. +  
seagull  I should have clarified that I was speaking about mature B cells. Thank You +1  
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right? +  
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html +  
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above) +  


submitted by seagull(437),

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD). +2  
hungrybox  To clarify - immature B cells have antibodies attached to their membrane. +  
seagull  I should have clarified that I was speaking about mature B cells. Thank You +1  
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right? +  
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html +  
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above) +  


submitted by assoplasty(41),

I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.

When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.

The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +3  
arkmoses  great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down! +2  
whoissaad  you mean total amount of T4 is "not changed"? 2nd para last sentence. +  
ratadecalle  @whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well. +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  


submitted by hayayah(416),

the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.

The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.

hungrybox  Amazing explanation. Thank you!! +  
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png +3  
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +  


submitted by hajj(0),

can anyone explain this? i know median for y is higher by calculation but x has two modes so how come y has higher mode?

lispectedwumbologist  The mode in X is 32 and the mode in Y is 80 +  
lispectedwumbologist  The mode in X is 70 and the mode in Y is 80* +1  
hajj  Thank you! +  
hungrybox  Just checking in so I could feel smart about getting this right despite bombing the rest of the test lmao +2  
usmleuser007  can someone please explain the median in this +  
nala_ula  The median can be known by first assembling the numbers in order from least to greater. If it's an uneven number set, the number in the middle is the median (for example: 4, 10, 12, 20, 27 = median is 12 since this is the number in the middle); if the numbers are even then you have to take the two values in the middle, add them up and divide them by 2 [for example: 4, 10, 12, 12, 20, 27 = (12+12)/2 = 12]. Page 261 on FA 2019 explains it as well. Not sure if I explained it well... good luck on the test, people! +  
dubin johnson  Can someone please explain how the mode for Y than X. Not sure how we got the values above. Thanks! +  
dubin johnson  I mean how is the mode for Y greater than mode for x? +1  
sgarzon15  Mode is the one that repeats the most once you list them in order +  
usmile1  Median would be the BP value that the person in the 50th percentile of each group would have. So for group X, to find the 50th percent value, I added 8 + 12 + 32 = 52, which is right above 50, so the median would be 70 mmHg for group X. Doing the same thing for group Y, 2+8+10+20+ 18 = 58; the 50th percentile would fall in group that had a BP of 90 mmHg. which makes the median higher for group Y. hope that isn't wrong, and helps someone! +4  


submitted by beeip(63),

I might be the only person on earth who got this one wrong, but regardless:

"ITT analysis includes every subject who is randomized according to randomized treatment assignment. It ignores noncompliance, protocol deviations, withdrawal, and anything that happens after randomization."[1]

yo  You're not. I also goofed. +3  
seagull  https://www.youtube.com/watch?v=Kps3VzbykFQ This video is a pretty decent explination worth your time on the subject. +2  
hungrybox  I got it right but I was only like 50% sure. So I appreciate it. +  


submitted by feronie(6),

Orchiectomy = ↓ testosterone production = ↓ DHT => prostate cells undergo apoptosis. (This mechanism is similar to using 5α-reductase blockers to treat BPH.)

Apoptosis is characterized by DNA fragmentation (pyknosis, karyorrhexis, karyolysis).

hungrybox  DNA fragmentation histopath: https://i.imgur.com/nxYW8vL.png Note that degradation in apoptosis is progressive. From pyknosis -> karyorrhexis -> karyolysis. Aka condensation -> fragmentation -> complete dissolution. +5  


submitted by hungrybox(241),

ethambutol = EYEthambutol

Great mnemonic for remembering that EYEthambutol is the component that causes visual problems in RIPE therapy for TB.

hungrybox  RIPE = rifampin, isoniazid, pyrazinamide, ethambutol +  


Candida is a part of the normal flora of skin, could cause contamination of a central venous catheter. The question states that the organism is purple, budding, did not respond to broad spectrum antibiotics (aka they didn't use fluconazole or amphotericin B). Lastly, they showed it plated on blood agar and there was no hemolysis which eliminates staph (the only other possible contender here.)

Cryptococcus usually involves meningitis in immunocompromised pts. E. coli is gram negative sporothrix is usually transmitted by a thorn on a rose or someone with a history of gardening

hungrybox  Also, the yeast form of Candida is gram (+) +4  
dr_jan_itor  I got thrown off by the part where they said "ovoid" and thought they were implying a cigar shape. I chose sporothrix for the morphology in spite of knowing that it clincally made no sense. +  
lilmonkey  I chose S. aureus before reading the question (looks like b-hemolysis). Then I saw "budding organisms" and picked the correct one. +  


submitted by drdoom(211),

Here’s one way to process-of-eliminate “decreased hydrogen-bond formation”: I’m not a big fan of this line of reasoning, but technically alanine as a side group has more hydrogens* for potential hydrogen bonding than glycine:

alanine: —CH3
glycine: —H

So, “technically,” alanine would permit more hydrogen-bond formation, which might allow you to eliminate that choice.

That said, it seems almost impossible to rule out (without very technical knowledge or some provided experimental data) that the slightly larger alanine does not impair hydrogen bonding between collagen molecules via steric (spatial) interference. In simpler terms, since alanine is larger, you would think that it must somehow interfere with the hydrogen-bonding that occurs with the wild-type glycine.

---
*Strictly speaking, it’s not the number of hydrogens but also the strength of the dipole that facilitates hydrogen bonding: a hydrogen bound to a strongly electronegative molecule like fluorine will “appear” more positive and, thus, hydrogen-bond more strongly with a nearby oxygen (compared with a hydrogen connected to carbon, for example).

Further reading:

  1. https://www.chem.purdue.edu/gchelp/liquids/hbond.html
hungrybox  Appreciate the effort but this is far too long to be useful. +1  
drachenx  hungrybox is a freaking hater +  
drdoom  @drachenx haha, nah, coming back to this i realize i was probably over-geeking lol +  


Membranous Glomerulonephritis is Nephrotic; ONLY PROTEINURIA is in the vignette

It can't be MPGN because MPGN is Nephritic with possible Nephrotic

Other choices are eliminated by Renal Biopsy

hungrybox  agreed "granular deposits" rules out MCD (the only other nephrotic syndrome) because MCD is IF (-) +2  
cooldudeboy1  could someone explain why the other choices are ruled out by biopsy? +