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Welcome to krewfoo99's page.
Contributor score: 58

Comments ...

 +2  (nbme18#21)

Calcium Carbonate is an antacid which can chelate and decrease effectiveness of other drugs such as tetracyclines and fluroquinolones

 +3  (nbme24#33)

HPV has high affinity for squamous epithelium. True vocal cords have squamous epithelium, thus HPV tends to grow there

suckitnbme  Specifically stratified squamous epithelium I believe.

 +0  (nbme24#33)

Basically, acute prostatis is caused by organisms which cause UTI also.

 -3  (nbme24#50)

This could easily be confused with Squamous Cell Carcinoma as they are describing a mass. But i think the key difference is that they mention METAPLASIA. If it was dysplasia, then it would have been cancer.

usmlecrasherss  metaplasia also can lead to cancer FA p206 2019
suckitnbme  Dysplasia is not cancer since it is, in theory, still reversible. Only when it becomes irreversible is it a carcinoma.

 +1  (nbme24#1)

folic acid when it enters the body is in the form of methyltetrahydrofolate (THF methylated). It donates its methyl group to vitamin B12 to become THF (the active form which as a DNA precursor). The vitamin B12 with its methyl group goes on to combine with homocyteine to form methionine.

 +0  (nbme24#2)

Lung volume will decrease in obesity hypoventilation syndrome. Even though this patient is obese, he has all the clinical features of sleep apnea

 +6  (nbme24#4)

If you ever get confused with the diagram remember:

CN 1,2,3,4 - Midbrain CN 5,6,7,8 - Pons CN 9,10,11,12 - Medulla

Since only one structure in the diagram is coming out of the medulla then it has be the vagus nerve

 +2  (nbme24#17)

Why would decreased movement through the cerebreal aquaduct be wrong? With all the build of blood in the CSF tract without absorption, wouldnt movement also be decreased through the aqueduct?

ergogenic22  this would cause a non-communicating hydrocephalus with enlarging of the lateral and 3rd ventricles but normal 4th ventricle and subarachnoid space

 +0  (nbme24#41)

I think chloroquine resistance wont be specefic to vivax and ovale,thus making it the incorrect answer. Chloroquine resistance can apply to P. Falciparum and P. Malariae

Only vivax and ovale cause hypnozoite thus making that the more clear answer

 +1  (nbme24#22)

EBV virus infections B cells. As a response there is reactive lymphocytosis (proliferation of CD8+ cytotoxic T Lymphocytes). In HIV, you will have a decrease in TH cells leading to decrease in CD8 T cells. Thus EBV will proliferate more freely as the immune response towards it (CD8 cells) are blunted. This is how i got to the answer.

 +2  (nbme24#3)

NRTI - Bone marrow supression, Lactic Acidosis, Anaemia NNRTI - Hepatotoxicity, rash Integrase inhibitor (tegras) - Myopathy (causing Increased Creatinine Kinase) Protease Inhibitors (navir) - Lipodystrophy, Hyperlycemia, GI intolerance (think of hormonal effecs)

madojo  building off on this... answer choice A would be something like Maraviroc, and B is basically the same thing as A because a fusion inhibitor would be something like Maraviroc where you don't have any interaction with CCR5 and gp120.

 +2  (nbme23#35)

Image shows Stahorn Calculus

1) Staghorn Calculus in adults - Manesium Ammonium Phosphate 2) Staghorn Calculus in Children - Cystine

 +1  (nbme23#22)

Why would perforins be the wrong answer? Wouldnt accumulation of toxic proteins cause the cell to undergo apoptosis ?

ergogenic22  Bortezomib does not directly activate perforin. It directly inhibits the proteasome which → enables CD8+ T cells to initiate apoptosis → via perforin release (in essence a downstream effect).
drzed  Exactly, it triggers the cells to undergo apoptosis which means that it can either be cell mediated (perforin and granzyme via FAS/FASL) OR it could also be through the intrinsic pathway (e.g. mitochondrial; cytochrome c)
powerhouseofthecell  Question: But how do CD8 cells have a role in this process exactly in the vignette? Is it saying that when the proteins build up, only then do CD8 cells come and instead of MHC I presenting to proteasomes, they present it to CD8 to initiate apoptosis?

 +8  (nbme23#19)

So basically what this is saying that DNA will be transmitted to the progeny not RNA. So DNA will replicate in the G2 phase and transfer of DNA material to progeny will occur in the M phase. The RNA may be mutated and making defective products, but this will not transmit into the progeny, thus not affecting species survival based on RNA mutations.

bk2458  makes sense!!
almondbreeze  good work
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know...
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny.

 +1  (nbme23#33)

In what situations will HbH be formed (3 alpha chain deletions)?

ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent
ergogenic22  ↑↑ I made a mistake by confusing trans and cis cis has deletions on the same chromosome and can pass two deletions to off spring, therefore a chance of allowing HbH

 +0  (nbme23#28)

Can someone explain what the picture is supposed to show? Is it supposed to be segmented neutrophils?

titanesxvi  yes do to B12 deficiency

 +6  (nbme23#50)

Afterload and heart rate share an inverse relationship.

As the umbilical cord is compressed, there is an increase in systemic vascular resistance (Think of how the pressure would increase if you were to press down on a water hose). Thus, the afterload is increased and there is a compensatory decrease in heart rate.

divya  yeah, i too thought similarly. btw increase afterload --> increase in bp --> baroreceptor firing --> decrease in heart rate. is that it?

 +1  (nbme23#12)

Wouldnt the HCOM murmur be best heard in the aortic area?

krewfoo99  Correction: Shouldnt it be heard best in the left upper sternal border?
usmlehulk  In FA 2018 page 303. patients with HOCM presents with MItral regurgitation due to impared mitral valve closure. Hence this explains the murmur.

 +3  (nbme23#49)

Epinephrine acts mostly on Beta receptors. Beta receptors are G coupled.

baja_blast  Alpha receptors are also G-coupled and are another potential site of action for Epinephrine (at high doses according to SketchyPharm Sympathomimetics)

 -2  (nbme23#21)

My reasoning:

As you go below sea level, there is an increase in atmospheric pressure. Increase in the pressure may cause rupture of subpleural blebs leading to pneumothorax.

Not sure if this is entirely correct though.

 +0  (nbme23#23)

Anyone know why heart sounds would be distant in COPD exacerbation?

yng  Patient is usually obese (blue bloater) --> diaphragm movement is limited --> can't take deep breaths, and in extreme cases, the chest size increased and causing distant heart sound.

 +0  (nbme23#23)

Anyone know why heart sounds would be distant in COPD exacerbation?

marat  Cause lungs are overextended
marat  overexpanded

 +1  (nbme23#41)

In boards and beyond, It is said that third degree heart block is due to block in the HIS Purkinjee system. So why would ablation of AV node cause this disease?

Wouldnt destruction of part of left ventricle be a better answer ?

brbwhat  Had the same doubt, Read the part again and found this. Type 2 Is caused when purkinje is hanging by a thread and therefore some impulses conducted, some not. Chb is caused by purkinje not conducting impulses from san, some lower pacemaker ie purkinje or his is depolarising by itself hence venrticles beat independently. There is BLOCK in purkinje for conduction from san. Among options the only thing that establishes this block is avn ablation.

Subcomments ...

submitted by seagull(840),

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +4  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +2  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +3  
pg32  I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them. +1  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +3  
jackie_chan  Not true, the logic works. You gotta know what aspirin does at least, it interferes with COX1 irreversibly and inhibits platelet aggregation (kinda like an induced Glanzzman), all it does. PT, aPTT are functions of the coagulation cascade and the test itself is not an assessment of platelet function. Bleeding time/clotting time is an assessment of platelet function. A- decreased plasma fibrinogen concentration- not impacted B- decreased aPTT/partial- DECREASED, indicates you are hypercoaguable, not the case C- decreased platelet count- aspirin does not destroy platelets D- normal clotting time- no we established aspirin impacts clotting/bleeding time by preventing aggregation E- prolonged PT- answer, aspirin does not impact the coagulation factor cascades in the test +  
teepot123  di'coumarin'ol +  

submitted by seagull(840),

Im also convinced blocking IL-2 is also a treatment? WHy is TNF-alpha the better answer here?

amorah  FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically. +8  
sbryant6  Spot on. This image explains how Sirolimus blocks the effects of IL-2: https://image.slidesharecdn.com/11-150813013011-lva1-app6892/95/11immunosuppressants-30-638.jpg?cb=1439429471 +  
krewfoo99  in addition to the above responses, IL 1 antagonists (Anakinra) can be used to treat RA. Anakinra is a recombinant human IL 1 receptor anatagonist but less effective than other treatment modalities. +  
snripper  Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option. +  

submitted by sunny(-1),

why is this so //i know its basic but still...??

krewfoo99  I think its neutrophils because they mention myelosupression and rapidly dividing cells. +  
wishmewell  Ya, Neutrophils, basophils, macrophages, eosinophils are considered Myeloid cells. While the rest of the T cells are from the Lymphoid lineage, The Immunoglobulins come from B cells ( lymphoid lineage). +1  

submitted by m-ice(236),

Misoprostol is a prostaglandin analog (PGE2) that acts on the stomach to promote mucus protection of the stomach lining, but also acts in the uterus to encourage contraction, which makes it useful for abortion.

usmile1  perfect except it is a PGE1 analog, not 2 +2  
krewfoo99  PGE2 will increase uterine tone (Pg. 270 FA 2018) +  
drmohandes  Misoprostol prevents NSAID-induced peptic ulcers. Side-effect: also gets rid of baby. +  

in the other hand , urine potassium is high enough , so if seizures =>rhabdomyolysis => myoglobinuria => ATN => high potassium excretion , why not?

krewfoo99  True but hypokalemia would occur in the recovery phase. So weeks after the inciting phase. +1  
therealslimshady  Acute rhabdomyolysis would lead to hyperkalemia, not hypokalemia, because cells are packed with K+ +  

submitted by zbird(2),

This patient has Distal-Type I RTA which is explained by Normal Serum Anion gap (8) Metabolic acidosis with her positive urinary anion gap(+5).

krewfoo99  Why would the urine Potassium be so high if it is type 1 ? Shouldnt it be type 2? +  
drpatinoire  @krewfoo99 I think it's RTA2 (Fanconi syndrome), he is losing all kinds of Na, K, Cl which should be reabsorbed in PCT. +  
misterdoctor69  @Drpatinoire: it can't be RTA2 because the urine anion gap (UAG) is positive (+), which implies that the patient is unable to secrete H+ (via NH4+, which couples w/ Cl-). RTA2 on the other hand has a negative (-) UAG because RTA2 affects only the proximal tubule's ability to reabsorb bicarbonate (i.e. H+ secretion via NH4+ in the distal convoluted tubule is unaffected). +  

submitted by roygbiv(17),

Why could this not be extravascular hemolysis? In FA it says acute hemolytic transfusion reaction can be due to ABO incompatibility or extravascular hemolysis.

niboonsh  because extravascular hemolysis is associated w jaundice. Intravascular hemolysis would have hemoglobinuria but that's not an answer +  
niboonsh  i mean that is the answer lol +  
krewfoo99  According to pathoma: Intrvascular haemolysis will lead to haemoglobin binding to haptoglobin. This complex will travel to the kidneys and be excreted. This will lead to red colored urine and haemosiduria (Note: This can also lead to acute tubular necrosis) Extravascular haemolysis is when macrophages break down the RBC. Then the Haeme is converted to biliverdin then bilirubin and conjugated in liver, and then excreted. +3  
paperbackwriter  If you look under the "clinical presentation" column of the blood transfusion reactions chart (pg114), it says that hemoglobinuria is with intravascular hemolysis and jaundice is with extravascular. Makes sense because with extravascular hemolysis your splenic macrophages are are chewing up the RBCs and sequestering it in the spleen so you don't get "spillover" -- i.e. clean urine. +1  

submitted by medskool123(17),

how did you know it was a strawberry hemangioma and not a port wine stain?I thought I had this one in the bank

kateinwonderland  Me too! TABLE 1 Classification of Vascular Lesions Vascular malformations (flat lesions) -Salmon patch (also known as nevus simplex or nevus telangiectaticus) -Port-wine stain (also known as nevus flammeus) Hemangiomas (raised lesions) -Superficial hemangioma (also known as capillary nevus hemangioma) -Deep hemangioma (also known as cavernous hemangioma) https://www.aafp.org/afp/1998/0215/p765.html +  
krewfoo99  Because they describe the lesion as cavernous vascular channels +  
covid2019  After looking into it, port wine stain comes as part of Sturge Weber SYNDROME. Given that this child was coming in for a well-child examination, they're implying there's no other symptoms (SWS would have signs of other vascular malformations like in the CNS--> epilepsy). +  

submitted by whoissaad(47),

What guarantee do we have that the roommate is going to stop smoking in the apartment by "asking" him to do so..?

krewfoo99  There is no guarentee. They are basically asking what a trigger is for her asthma recurrence. Smoking in this scenario can be the cause of this patients symptoms. Dont dwell to deep into the question. +1  

submitted by seagull(840),

A- primary motor cortex = wrong side of body (deficit of UMN on left side body)

B - Thalamus = sensory information conduit - motor deficits unlikely to originate from here

C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on right side + facial features.

D. Vermis - central body coordination. Damage results in ataxia

Not complete but maybe helpful..

yotsubato  C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on LEFT side + RIGHT sided facial features. Decussation occurs in medulla +1  
kard  Sorry if im mistaken, Isnt A) Somatosensory? +1  
krewfoo99  Yes i think A should be somatosensory. Primary motor cortex would be present in the precentral gyrus +  
drpatinoire  A is primary motor. A and the gyrus at right side of A compose the paracentral lobule. +  

submitted by m-ice(236),

Competitive inhibitors increase the Km of the substrate. The Km represents how easily a substrate can bind the active site, with a lower Km representing easy binding, and a higher Km meaning more difficult. If you add a competitive inhibitor, like ethanol in this case, it makes it more difficult for the methanol to bind the active site, because it must compete with the ethanol.

deathbystep1  but how is ethanol a "inhibitor" of alcohol dehydrogenase? isnt the concept that both ethanol and methanol compete for the same binding site of alcohol dehydrogenase and hence ethanol displaces methanol preventing its metabolism? if ethanol were to be a inhibitor it would have to shut off the enzyme, which is does not. +  
krewfoo99  @deathbystep1 Competitive inhibitor simply means increasing concentration of a particular substrate will allow more binding of the substrate to the enzyme. Thus the substrate with the higher concentration will competitive inhibit the other substrate by binding to the enzyme. It dosent necessarily shut off the enzyme +1  

out of curiosity, why are AST and ALT high? is that saying the NRTI used was diadenosine which led to pancreatitis also?

krewfoo99  AST and ALT will not be elevated in pancreatitis, they will only be increased during liver damage. NRTI causes hepatoxicity (although FA 2018 states NNRTI causes hepatotoxicity, NRTI could also be an option considering the two classes are similar. The hepatoxicity will cause an increase in ALT and AST +  

The disease here is fructose bisphosphatase deficiency. In it, IV glycerol or fructose doesn’t help because both enter the gluconeogenesis pathway below fructose bisphophatase. Galactose on the other hand enters above it. I don’t think you really need to know this to choose the correct answer since the clinical picture of fasting hypoglycemia that is corrected w/ some sort of sugar that can enter the gluconeogenesis pathway should clue you into the right answer.

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +15  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +17  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
mdrahimi7  See linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose b is phosphatase +  
mdrahimi7  See @linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose bis phosphatase. +  

submitted by m-ice(236),

This woman has Paroxysmal Nocturnal Hemoglobinuria. This most often presents in a young adult who has episodes of dark urine in the middle of the night or when waking up in the morning. It's caused by complement activity directly against the patient's own RBCs. Certain glycolipids are needed on the RBC surface to prevent attack from complement, the most notable of which are CD55 and CD59. Patients with PNH have a somatic mutation in which they lost function of a PIGA enzyme needed for proper presentation and attachment of CD55/CD59 on the RBC surface. Therefore the answer is a defect in a cell membrane anchor protein. Without this, complement attacks RBCs.

usmleuser007  I knew the disorder and its pathophysiology. But sometimes the answer choices are so wordy or colorful that you still get it wrong.... +12  
sunshinesweetheart  I got this one right but now upon review I'm having trouble ruling out hereditary spherocytosis ("abnormal cell morphology") answer choice. It helps that the dark urine is in the mornings, but is it officially ruled out because of her age? like this is obvi an acquired mutation if someone's 33? +  
krewfoo99  @sunshinesweetheart Hereditary Spherocytosis is a autosomnal dominant condition. The patient in the question stem has had dark urine since the past 2 months (acute presentation). Since spherocytosis is hereditary, it wont be present as a acute condition +4  

submitted by colonelred_(79),

Attributable risk = incidence in exposed – incidence in unexposed

= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)

Applying it to a population of 10,000:

= 0.02 * 10,000
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +2  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +1  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +4  

submitted by hayayah(883),

Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.

  • Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.

  • Colobomas involving the retina result in vision loss in specific parts of the visual field.

  • Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.

mousie  thanks for this explanation! +  
macrohphage95  can any one explain to me why not lens ? +  
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +2  
qfever  Do anyone know why not choroid? +  
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2  
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up +1  
mnemonicsfordayz  Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO. +  

submitted by amarousis(15),

But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.

krewfoo99  It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive) All three of the tracts are affected in Friedrichs Ataxia +  
krewfoo99  Sorry. Just checked on FA. It will also affect the spinocerebellar tract +  
spow  Sensation to pinprick is DCML +  

submitted by amarousis(15),

But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.

krewfoo99  It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive) All three of the tracts are affected in Friedrichs Ataxia +  
krewfoo99  Sorry. Just checked on FA. It will also affect the spinocerebellar tract +  
spow  Sensation to pinprick is DCML +  

submitted by notadoctor(121),

According to Goljan, polycythemia vera is one of the most common causes of Budd-Chiari syndrome. According to FA, Budd-Chiari is associated more generally with hypercoagulable states, polycythemia vera, postpartum states, and HCC.

Hepatic cirrhosis can be ruled out based on the time course of the patient's presentation - he was fine 2 weeks ago and the abdominal pain started an hour ago.

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1  
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +1  

The way I excluded vasodilation was this: the sympathetic receptor that dilates is β2, which is not stimulated by norepinephrine. So to stimulate the receptor, the stellate ganglion would have had to first stimulate the adrenal medulla to release epinephrine (stellate too high to stimulate the medulla).

shriya goyal  nice explanation +1  
shriya goyal  nice explanation +  
shriya goyal  nice explanation +  
shriya goyal  nice explanation +  
krewfoo99  But isint beta 1 (heart rate) also stimulated by Epinephrine? +  

submitted by welpdedelp(154),

Hemochromatosis, aka "bronze diabetes". Cannot be Addison due to the hyperglycemia and normal BP

alexb  I missed this bc didn't notice it was a middle-aged guy w/ just 3 year hx of Type 1 DM. +2  
tinydoc  I got it mixed up with primary adrenal insufficiency and the acth ⇒ hyperpigmentation. +9  
maddy1994  testicular atrophy &hepatomegaly helped me out to eliminate the options..when i was left with ferritin and saw pigmentation it clicked that it is hemochromatosis +3  
krewfoo99  Symptoms of Darkening of skin, liver dysfunction, diabetes, with testicular atrophy will always be hemochromatosis +2  

submitted by krewfoo99(58),

Wouldnt the HCOM murmur be best heard in the aortic area?

krewfoo99  Correction: Shouldnt it be heard best in the left upper sternal border? +  
usmlehulk  In FA 2018 page 303. patients with HOCM presents with MItral regurgitation due to impared mitral valve closure. Hence this explains the murmur. +  

submitted by kimcharito(7),

it is normal irradiation to the RIGHT neck? what does it mean?

krewfoo99  @kimcharito Aortic stenosis radiates to the carotids FA pg. 285 (2018) +1  

submitted by sajaqua1(389),

Because the baby's mother has Type 1 Diabetes mellitus, it is plausible that they had elevated blood glucose levels during or shortly before birth. Insulin does not cross the placenta, but glucose does, so during birth the neonate would have been hyperglycemic. This would lead to the neonatal pancreas releasing insulin, driving glucose into cells and turning down gluconeogenesis; this is why the baby is hypoglycemic right now.

B) Decreased glycogen concentration- I don't know the glycogen concentration compared to an adult patient, but a decrease in glycogen concentration would indicate glycogen/glucose release, which would not be a hypoglycemic state. C) Decreased glycogen synthase activity- decreased glycogen synthase activity indicates energy catabolism, and would lead to higher serum glucose levels. D) Decreased serum insulin concentration- decreased serum insulin would lead to higher levels of glucose in serum. E) Increased serum insulin-like growth factor- IGF does not bind nearly as well to insulin receptors as insulin does, and so would have to be in extremely high concentrations to have this effect. IGF is associated with somatic growth and muscle development.

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
alexb  Also explains why he's 12 pounds. +2  
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite +1  
tyrionwill  fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia. +  

The question says they don't responds to antacids THEN asks which you to identify which drug is the most effective at suppressing acid production, NOT what the most effective antacid is. The answer is PPI's.

I will say, however, I was looking for something like octeotride.

drdoom  lucid. nice catch. +1  
maddy1994  WHY not blockage of h2 receptors +1  
krewfoo99  @maddy1994. PPI are more effective than H2 blockers in suppression of gastric acid +1  

submitted by aladar50(33),

I’m not the best at the calculations of ICF/ECF, but basically you are infusing a hypertonic solution into the animal. Initially, this is all going to go into the extracellular space, as any IV infusion will do. Since it is higher than isotonic solution, water is going to go from the intracellular space to the extracellular space to try to balance it out, so the intracellular space will have decreased volume and increased osmolality (since only water is leaving, making it more concentrated).

So you know for sure ICF volume is decreased and osmolality increased, and the extracellular volume will be increased. I think the osmolality of the extracellular space is the tricky part and the part where maybe someone else can help with the calculations but basically it’s hypertonic enough that the osmolality will still be increased.

btl_nyc  Since hypertonic solution was added, osmolality has to go up. The degree of the hypertonicity doesn't really matter. The fluid flowing out of the ICF will increase ICF osmolality. Since water follows salt, the water's gonna flow only until the ECF and ICF have the same tonicity. So if the ICF osmolality went up, the ECF osmolality also had to go up, because they both need to be equal after the water is done equilibrating. +10  
krewfoo99  ECF fluid is hypertonic because we infused an hypertonic solution. ECF volume is going to go up because A) we added more volume via injection B) Sodium attracts water, and since hypertonic solution was given water goes from ICF to ECF ICF volume decreases because the water is going to ECF. This causes an increase in Intracellular osmolarity, since you have more solutes compared to water (Less water to dilute it) +  

submitted by jrod77(21),

I think they might be describing angina...not sure. TXA2 is responsible for platelet aggregation,so it may be contributing to thrombosis, thus ischemia to the cardiac tissue.

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +17  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +2  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +1  
shriya goyal  same I went for pgE2 ... I M PISSED +1  
shriya goyal  same I went for pgE2 ... I M PISSED +  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +3  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +4  
ususmle  same here I M PISSED PGE2 +1  
krewfoo99  Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +1  
djtallahassee  ditto on the looked at it for 2 seconds and went PGE2 +  

In addition to the previous explanation:

She is iron deficient and celiac affects the proximal duodenum. "I Fucked Brittany" = Iron, Folate, B12 for Duodenum, Jejunum and Ileum

krewfoo99  Great analogy lol. But just a correction, First Aid states that Celiac Disease affects distal duodenum and proximal jejunum. But you are right, it would still cause iron deficiency anemia as it affects the duodenum. +1  
fexx  OR you could just remember 'Iron Fist Bro' (F includes folate and fat, B includes B12 and bile salts) +  

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