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Welcome to topgunber’s page.
Contributor score: 10


Comments ...

 +0  (nbme16#4)

costochondritis is inflammation of the joints of the rib cage.(An inflammation of the cartilage that connects a rib to the breastbone). pain is reproducible with palpation, worse with movement and can be sharp in character. most importantly cardio / pulmonary findings will be negative.


 +0  (nbme16#4)

costochondritis is inflammation of the joints of the rib cage.(An inflammation of the cartilage that connects a rib to the breastbone). pain is reproducible with palpation, worse with movement and can be sharp in character. most importantly cardio / pulmonary findings will be negative.


 +0  (nbme16#48)

hardest part for me was differentiating absence of schwann cells vs abnormal myeling sheaths. Schwann cells come from neural crest cells so we would expect to see other neural crest migration issues in my opinion. CMT disease has motor and sensory issues because PMP-22 peripheral myelinating protein is mutated. leads to abnormal myelination of the peripheral nerves. foot drop from sensory degradation, muscle atrophy from motoneuron involvement (also peripherally myelinated)

topgunber  foot drop from motor degradation , high stepping gait from sensory degradation. also associated with hearing issues. +

 +0  (nbme16#36)

another way to remember this is NERD. NSAIDs-exacerbated respiratory disease (NERD), when blocking COX there is shunting of the Arachadonic acid breakdown into the LOX (lipooxegenase pathway) which can cause build up of leukotrienes and cause an asthma-like condition.


 +1  (nbme16#14)

Genetics- The following is a helpful way to do all the allele frequency questions / carrier frequency questions.

  • AD : I = 2pq. The cases are in nearly all carriers (2pq). Most homozygotes die. (q^2)
  • AR : I = q^2 (the cases are ONLY shown in homozygotes). The carriers are 2pq

  • X linked : Boys : I = q . Boys carrying ONE allele are affected individuals. GIRL CARRIERS (heterozygous females) : I = 2PQ. This gets us to the answer. On the other hand AFFECTED GIRLS (incidence in girls) would be I= q^2 - extremely small (choice e)

topgunber  By the way allele frequencies if asked are finding just q. Most of the time P is close to 1. In this case P would be 1-1/100,000 = 99,999/100000 which is why you can usually exclude it from equations +

 +0  (nbme16#17)

Experiment is asking which would increase pulmonary lymph flow, which I interpreted as which of these increases blood flow/intravascular volume. Endothelin, phenylephrine, low o2 concentrations all cause vasoconstriction. Co2 unlike in other organs (i.e. brain, muscle) does not cause vasodilation in the lungs so i left this one to the side. IV saline will for sure increase intravascular volume and blood flow so I leaned more toward this. The other explanation made a good point about the albumin solution in that it may cause reabsorption due to a high oncotic pressure (i.e. with albumin)


 +0  (nbme16#20)

its an external hemorrhoid, pic is of an anus with a hematoma round the 7 o'clock position. there is pain and bleeding with wiping which points me toward an external hemorrhoid. with the other answer choices being infectious causes the only two left were venous htn and lymphatic obstruction. because increased straining and increased pressure on the inferior and middle rectal veins went with venous htn. (not to be confused with superior rectal vein which is linked to portal htn and internal/ painless hemorrhoids)





Subcomments ...

Natural transformation is when bacteria take up naked bacterial chromosomal DNA in their environment (usually from cell lysis). A cell "lysate" is what remains of bacterial genes when the bacteria is dead (can be extracted from bacteria, as shown here). The SHiN bugs all can undergo transformation. You know it is transformation even without knowing which bugs can do so because it doesn't take up the DNA when DNase is added (it kills any free environmental DNA in the lysate)

topgunber  just wondering why is plasmid transfer not a good option??? +  
m0niagui  Transduction requires the presence of a bacteriophage virus. Plasmid transfer requires two different live bacteria, point mutations will not occur across colonies so uniformly and neither will strand mispairing. +1  
shakakaka  @topgunber I think DNase wouldn't stop the process in case of plasmids +1  
topgunber  you're right in that DNAse wouldn't be able plasmids in living cells because they are inside the bacteria (same with their nuclear dna). Since living cells use sex pilli to transfer plasmids yes, DNAse wouldn't stop plasmid transfer. Key there is they had to be living. I do think a dnase can break down a plasmid in extracellular solution though (its just another piece of dna). +  


submitted by cassdawg(957),

Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]

Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.

lee280  For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks +2  
notyasupreme  I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it. +1  
topgunber  sildenafil does make sense, especially since hes on 2 vasodilators. I picked diltiazem because the pt has systolic heart failure. thought it was contra indicated to give CCB to systolic heart failure because you could further decrease contractility. Either way never give NTG and viagra +  


submitted by cassdawg(957),

He presents with an anticholinergic toxidrome: hot as a hare, dry as a bone, mad as a hatter (FA2020 p241, the anticholinergic toxidrome is the same as an atropine overdose and jimsonweed actually contains atropine).

The antidote for antichlinergics is phyostigmine, an acetylcholinesterase inhibitor that acts as an indirect cholinergic agonist. (FA2020 p240)

topgunber  physostigmine because its liposoluble and has central effects as compared to neostigmine +1  


submitted by cassdawg(957),

HbS homozygosity indicates Sickle Cell disease. Streptococcus pneumoniae is associated with sepsis in patients with Sickle Cell (due to autosplenectomy causing increased risk of infections with encapsulated organisms) [FA2020 p136 and 422]

Streptococcus pneumoniae is susceptible to penicillin and prophylactic penicillin can decrease risk of infection.

Sickle cell patients would also be at increased risk of infection with E.coli, H. influenzae and neisseria (as they are encapsulated, p127) but they run less of a risk than Strep pneumo than causing sepsis in sickle cell patients. Salmonella is the most common cause of osteomyelitis in sickle cell patients but again is not what we would primarily be concerned with in this baby.

https://pediatrics.aappublications.org/content/141/3/e20172182

selectuw  I believe Staph is the most common cause of Osteomyelitis in Sickle cell but Salmonella commonly causes it in them more than the general population. +  
fruitkebabs  @selectuw You have it backwards, S aureus is most common overall, while Sickle Cell patients are more likely to have Salmonella Osteomyelitis (and S aureus as well). As a separate note, I thought the answer was Salmonella because Sickle Cell patients are functionally Asplenic beginning age 2-4 (Amboss) since it takes time for all the vessels in the spleen to get occluded and undergo necrosis, esp while HbF is still around in the first 6 months. Maybe that's why this question was taken out of active rotation? +3  
i_hate_it_here  This question was annoying. Sickle cell patients are at risk for all encapsulated organisms, and penicillin is not the main-stay treatment for any of these bugs. Only got this question right because S. pneumo was the only gram positive +  
topgunber  think that was the purpose of the q honestly, they wanted you to pick salmonella for osteomyelitis, but logically penicillin's moa is targeting the only gram positive in the list. +1  


submitted by cassdawg(957),

Interviewing the subjects as a means of measuring the exposure introduces the risk of recall bias which would bias the measurement of the exposure. Recall bias occurs when individuals with a disease tend to recall exposure more in retrospective studies (FA2020 p260)

topgunber  example: pregnant women who had a drink while pregnant and had a kid with birth defects much more likely to report drinking than a woman who drank and didn't have a kid with a birth defect. thats the example our epidemiology prof gave us over and over. +  


Just wondering if someone could explain the difference between collagen and elastin for this one? I thought either or could be used for tensile strength. Anyone have clarification, don't know why collagen is the best answer!

notyasupreme  Lol, never mind I realize, it's a scar and that's type III collagen! +2  
meryen13  type III is whats usually present but then it gets replaced by collagen I in the scar tissue to add more strength. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352699/ +  
i_hate_it_here  It is also the disulfide bonds that add to tensile strength of collagen, while the inter-chain fibril cross-linking that leads to elastins elasticity FA2020 pg: 51&52 +  
xw1984  I think the Q emphasized postoperatiive. Maybe the production of elastin does not increase much comparing to collagen. +  
topgunber  i think they would refer to elastin in cases of arteriolar compliance +  


Child has albinism. Defective melanin synthesis due to deficiency of enzyme tyrosine hydroxylase. FA 2020, page 476

topgunber  tyrosinase. tyrosine hydroxylase would make L-dopa +1  
sabrooza  It is Tyrosinase deficiency not (Tyrosinase hydroxylase ) +  


Natural transformation is when bacteria take up naked bacterial chromosomal DNA in their environment (usually from cell lysis). A cell "lysate" is what remains of bacterial genes when the bacteria is dead (can be extracted from bacteria, as shown here). The SHiN bugs all can undergo transformation. You know it is transformation even without knowing which bugs can do so because it doesn't take up the DNA when DNase is added (it kills any free environmental DNA in the lysate)

topgunber  just wondering why is plasmid transfer not a good option??? +  
m0niagui  Transduction requires the presence of a bacteriophage virus. Plasmid transfer requires two different live bacteria, point mutations will not occur across colonies so uniformly and neither will strand mispairing. +1  
shakakaka  @topgunber I think DNase wouldn't stop the process in case of plasmids +1  
topgunber  you're right in that DNAse wouldn't be able plasmids in living cells because they are inside the bacteria (same with their nuclear dna). Since living cells use sex pilli to transfer plasmids yes, DNAse wouldn't stop plasmid transfer. Key there is they had to be living. I do think a dnase can break down a plasmid in extracellular solution though (its just another piece of dna). +  


submitted by cassdawg(957),

This is mesenteric artery stenosis causing postpranidal intestinal ischemia/angina. I definitely did not know this answering the question and I personally got to the answer by attempting to logically think through the symptoms:

  • Weight loss and abdominal pain in general pointed to intestinal ischemia of some sort and since most absorption of nutrients happens in the jejunum, ischemia there would cause weight loss. Jejunum is supplied by SMA
  • Bruit to me meant a larger vessel was blocked since to be able to hear it it has to be a pretty large vessel, SMA is one of the larger arteries listed
  • No liver symptoms (i.e. jaundice) so eliminated hepatic artery

If anyone has a better explanation please offer it.

deathcap4qt  great explanation for not knowing the answer! You're right in that it has to do with a vessel of a larger size. Generally Celia, SMA or IMA. pt hx of atherosclerosis should be a big hint. FA 2019 pg 380. +2  
nbmeanswersownersucks  SMA is the MOST COMMON vessel involved in ischemic bowel disease. +1  
baja_blast  I reasoned this out by remembering that the Abdominal Aorta was the most common place for atherosclerosis and picking the only option that branches off immediately from there. Not sure if that's what they were going for but it got me to the right answer. +1  
topgunber  i think thats a great explanation ^, namely because its possible obstruction at the other vessels may not cause symptoms due to collateral circulation. SMA on the other hand, if stenosed, would have a number of regions with ischemia- not to mention its involved in a watershed area. +  


submitted by andro(172),

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

notyasupreme  It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me. +2  
nbmeanswersownersucks  yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine. +  
baja_blast  If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible? +5  
melanoma  the presence of dicarboxylic aciduria is more related to mcad/lcad deficiency. the patient receives medium chain tryglicerides because he has the enzyme to metabolize it. +2  
melanoma  but no for the long chain +  
topgunber  just a few things, sure it sounds like mcad but lcad would present similarly, except in MCAD, giving medium chain triglycerides would worsen symptoms as compared with LCAD. + Similarly when fatty acids cant undergo Beta oxidation they undergo omega oxidation- which is why there is increased dicarboxlic acids (i.e. dont just jump for MCAD when you see dicarboxilic acids). Last of all it would be difficult to differentiate but if the patient were deficient in carnitine the treatment with MCADs would not show improvement because carnitine is required to shuttle the fatty acid into the MTs. +1  
topgunber  'a 'weird question' because my school never asked it' +1  


submitted by andro(172),

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

notyasupreme  It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me. +2  
nbmeanswersownersucks  yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine. +  
baja_blast  If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible? +5  
melanoma  the presence of dicarboxylic aciduria is more related to mcad/lcad deficiency. the patient receives medium chain tryglicerides because he has the enzyme to metabolize it. +2  
melanoma  but no for the long chain +  
topgunber  just a few things, sure it sounds like mcad but lcad would present similarly, except in MCAD, giving medium chain triglycerides would worsen symptoms as compared with LCAD. + Similarly when fatty acids cant undergo Beta oxidation they undergo omega oxidation- which is why there is increased dicarboxlic acids (i.e. dont just jump for MCAD when you see dicarboxilic acids). Last of all it would be difficult to differentiate but if the patient were deficient in carnitine the treatment with MCADs would not show improvement because carnitine is required to shuttle the fatty acid into the MTs. +1  
topgunber  'a 'weird question' because my school never asked it' +1  


submitted by topgunber(10),

hardest part for me was differentiating absence of schwann cells vs abnormal myeling sheaths. Schwann cells come from neural crest cells so we would expect to see other neural crest migration issues in my opinion. CMT disease has motor and sensory issues because PMP-22 peripheral myelinating protein is mutated. leads to abnormal myelination of the peripheral nerves. foot drop from sensory degradation, muscle atrophy from motoneuron involvement (also peripherally myelinated)

topgunber  foot drop from motor degradation , high stepping gait from sensory degradation. also associated with hearing issues. +  


submitted by topgunber(10),

Genetics- The following is a helpful way to do all the allele frequency questions / carrier frequency questions.

  • AD : I = 2pq. The cases are in nearly all carriers (2pq). Most homozygotes die. (q^2)
  • AR : I = q^2 (the cases are ONLY shown in homozygotes). The carriers are 2pq

  • X linked : Boys : I = q . Boys carrying ONE allele are affected individuals. GIRL CARRIERS (heterozygous females) : I = 2PQ. This gets us to the answer. On the other hand AFFECTED GIRLS (incidence in girls) would be I= q^2 - extremely small (choice e)

topgunber  By the way allele frequencies if asked are finding just q. Most of the time P is close to 1. In this case P would be 1-1/100,000 = 99,999/100000 which is why you can usually exclude it from equations +  


submitted by bingcentipede(217),

Dudes and dudettes, let me tell you how high yield Pathoma Ch. 1-3 are. Dr. Sattar is the freaking man.

Anyway, this is reversible cell injury because of swelling. If the Na/K ATPase is not working, Na is not leaving. Na follows water, so water is getting stuck in the cell, leading to swelling.

Most important is recognizing that it's reversible cell injury - everything else (except PFK lol) is talking about cell death

cassdawg  Love this explanation lol Dr. Sattar for president. FA2020 p207 for anyone who wants more details. +3  
the_enigma28  Ribosomal disaggregation (detachment) does occur in reversible cellular injury, but that is not the mechanism of cellular swelling! +1  
topgunber  this last comment is extremely important to recognize when asking about reversible injury +  


submitted by bingcentipede(217),

Although they had statistical significance with a p=0.001, it doesn't matter to the subjects. They're only falling asleep 5 minutes faster, and are personally not reporting an improvement in quality of life. So, clinically, this medication doesn't matter to the subjects because 5 minutes faster might not be that big of a deal.

It's not attrition bias because the threshold there is 5%. Here, 20/2000 subjects (1%) are lost, having little effect on attrition. Additionally, the acceptable range for bias is between 5-20%, which this doesn't approach. https://catalogofbias.org/biases/attrition-bias/

topgunber  The study has statistical significance. The study has no clinical significance because a) no improvement in QOL and b) 5 minutes faster than people with insomnia. +  


submitted by kding247(2),

Dr. Jason Ryan from BB emphasized that just because something is statistically significant, does not automatically mean it is clinically significant!

topgunber  god bless Dr. Jason Ryan. just about every teacher in med school has said the same. shame nobody gives them a chance +  


submitted by cassdawg(957),

In agreement with the other post: (see FA2020 p331)

You would want to check FREE T4 because pregnancy increases Thyroid binding globulin. It is possible she might have increased overall T4, but NOT have hyperthyroidism because the free T4 is normal (i.e. her increases amount of thyroid binding globulin has bound more T4, and since our bodies respond to the concentration of free T4 only, the hypothalamus should ensure that the free T4 is kept constant; this would appear as increased overall T4)

Another way of thinking of this:

  • Overall T4 = bound T4 + free T4

If we increase bound T4 and keep free T4 the same, we would still increase overall T4. Thus to know if she truly has hyperthyroidism we must look at free T4 concentration.

lpp06  Does Overall T4 stay the same because TBG+T4 can last longer in circulation? Cause I always struggle thinking that free T4 is low because its being bound by the extra TBG +  
covid_19  I'm not sure if I'm interpreting your question correctly, but I thought overall T4 increases in pregnancy? The way I think of it is that early in pregnancy, Ξ²-HCG (acting like TSH) β†’ ↑ free T4 β†’ ↓ TSH via (-) feedback β†’ TSH back to nml as ↓β-HCG during pregnancy (i.e. gestational thyrotoxicosis). If the mom really has hyperthyroidism, then free T4 remains high and TSH low even as Ξ²-HCG ↓ and ↑TBG. Later in the pregnancy, estrogen β†’ ↑TBG β†’ ↓ free T4 β†’ TSH release β†’ ↑ free T4 to regain equilibrium. (bound T4: free T4) 2:2 (nml) β†’ 3:1 β†’ 3:3 (new nml where there's a relative increase in free T4 AND overall T4). What are your thoughts on this? +  
topgunber  Overall t4 increases, but when t4 is bound to thyroid binding globulin it is not active, therefore someone would not show characteristics of hyperthyroidism if they had high thyroid binding globulin and high total t4. Basically, free t4 is the actual amount of thyroid hormone that can cause a physiologic effect. As the first comment says, total thyroid hormone and thyroid binding globulin are increased in pregnancy. Thus to check for hyperthyroid we are concerned only with free t4 (if it is low then the patient would be hypothyroid) +  


submitted by andro(172),

Patient with Primary Hypothyroidism (problem with the gland itself ) treated with T3

  • In normal physiology T4 is converted to T3 and less commonly ( rT3) . As such most of the T3 in the body is derived from the peripheral deiodination of T4 to T3
  • Also note that TSH secretion by anterior pituitary is under negative feedback control by both Free T3 and T4

So what happens when we give our Patient T3.
- firstly , we inhibit secretion of TSH from the pituitary gland . ( TSH decreases ).

This means less stimulation of the Thyroid and less hormone production . The Throid hormone it primarily makes and releases is T4 , ( and so T4 decreases ) . Naturally you would also expect a decrease in T3 but patient is taking exogenous T3( and so T3 increases )

schep  I messed this up because I know treatment of primary hypothyroidism is usually with levothyroxine (T4). I totally skimmed the part where we are told she is being treated with T3 +1  
jdc_md  ^nbme is asshoe! +1  
topgunber  side note thyroglobulin would also be low and is asked on uworld +1  
cheesetouch  Thyroxine = T4 +1  


submitted by andro(172),

Differential Diagnosis of Newborn/Neonatal Vomiting

-Benign gastroesophageal reflux ( i.e immature lower esophageal sphincter ) regurgitation of food shortly after feeding .
No further symptoms , healthy children with normal development

-Hypertrophic pyloric stenosis
Regurgitation - projectile nonbilious vomiting electrolyte imbalances ( alkalosis and hypokalemia ) * physical examination may reveal an olive mass on palpation of epigastrium
*typically starts from between 2nd and 7th week of age

-Midgut volvulus /Malrotation /Duodenal atresia * bilious vomiting * abdominal distention * Imaging may reveal signs like the double bubble sign ( duodenal atresia ) etc

Note: The list is not exhaustive as there are many more causes associated with newborn vomiiting

covid_19  To add on to Benign GER, I couldn't find anything in a cursory look through FA and also didn't know that GER was a thing in neonates, so I found this nice and concise article in UpToDate: https://www.uptodate.com/contents/gastroesophageal-reflux-in-premature-infants +  
i_hate_it_here  I don't understand why Esophageal spasm isn't right +  
topgunber  I would say esophageal spasm would cause immediate regurgitation or inability to swallow properly. so we would be looking for dysphagia. +1  


submitted by meryen13(13),

i was so confused by this question. is this because the rest are human antigens, so why would we have antibodies against them? but HPV is antibody toward E6 is foreign...?

topgunber  im going with this explanation. the rest : cd19, her2, Prostate acid phosph, tyrosinase are all endogenous molecules. makes sense that viral protein e6 has the highest immunogenicity. +2