Official Step 1 High Yield Concepts Thread

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Transposony

Transposony

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Let's discuss our doubts/offer clarifications about mechanisms/concepts for Step 1

ASK ANY QUESTIONS here.

To kick start the thread here is something I didn't know:

1. Penicillin-binding proteins (PBPs) are actually enzymes (transpeptidases & carboxypeptidases) which cross-link peptidoglycan. Penicillins binds to these enzymes and inactivating them thereby preventing cross-linkiing of peptidoglycan.

2. Periplasmic space (Gram -ve) contain proteins which functions in cellular processes (transport, degradation, and motility). One of the enzyme is β-lactamase which degrades penicillins before they get into the cell cytoplasm.
It is also the place where toxins harmful to bacteria e.g. antibiotics are processed, before being pumped out of cells by efflux transporters (mechanism of resistance).

There are three excellent threads which you may find useful:

List of Stereotypes

Complicated Concepts Thread

USMLE images
 
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From original post:

Name the cancer per the histology:

1) Fallopian-tube like epithelium; benign; female = ?
2) Bilateral, contains psammoma bodies = ?
3) Has intestine-like epithelium; loculated; female = ?
4) Papillary structures with fibrovascular cores; contains psammoma bodies = ?
5) Rows / distinct linearity of cells, bilateral = ?
6) Ataxia, dysarthria, nystagmus, oculomotor dysfunction, muscle rigidity in smoker with recent T2DM = ?
7) Varicocele in 60-year-old smoker = ?
8) I/VI holosystolic murmur at 2nd L-intercostal space in patient with ruddy appearance = ?
9) Perioral melanosis, palpitations, galactorrhea, echocardiography shows L-atrial mass = ?
10) Islands and nests of basophilic cells = ?
11) Cerebriform nuclei; infection with icosahedral, enveloped RNA virus that replicates in the nucleus = ?
12) 5-year-old boy; red face; leukocytosis = ?
13) Fever, bone pain, small blue cells = ?
Transposony said:
2) Bilateral, contains psammoma bodies = Serous cystadeno ca of ovary
7) Varicocele in 60-year-old smoker = RCC
9) Perioral melanosis, palpitations, galactorrhea, echocardiography shows L-atrial mass = Familial myxoma
10) Islands and nests of basophilic cells = BCC
Click to expand...
seminoma said:
1) Fallopian-tube like epithelium; benign; female = serous cystadenoma
3) Has intestine-like epithelium; loculated; female = mucinous cystadenoma
4) Papillary structures with fibrovascular cores; contains psammoma bodies = thyroid papillary carcinoma
11) Cerebriform nuclei; infection with icosahedral, enveloped RNA virus that replicates in the nucleus = Mycosis fungoides
Click to expand...
dfib slim said:
5) Rows / distinct linearity of cells, bilateral = NF2, bilateral schwannomas
8) I/VI holosystolic murmur at 2nd L-intercostal space in patient with ruddy appearance = Carcinoid metastasis
13) Fever, bone pain, small blue cells = Ewing's sarcoma
Click to expand...

2, 3, 4, 7, 8, 10, 11, 13 - yeah

11 can also be Sezary syndrome

9 = myxoma, but this is a specific constellation of symptoms (and showed up on my 2CK btw).
 
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6) Ataxia, dysarthria, nystagmus, oculomotor dysfunction, muscle rigidity in smoker with recent T2DM = SCC (Paraneoplastic)
12) 5-year-old boy; red face; leukocytosis = Erysipelas
 
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Transposony said:
6) Ataxia, dysarthria, nystagmus, oculomotor dysfunction, muscle rigidity in smoker with recent T2DM = SCC (Paraneoplastic)
12) 5-year-old boy; red face; leukocytosis = Erysipelas
Click to expand...

Erysipelas isn't cancer..

And yeah, Carney complex is #9. As I said, that showed up on my Step 2CK. FA and QBanks obsess over MEN1/2a/2b, but Carney complex is listed as a fourth MEN syndrome in the Johns Hopkins Internal Medicine board review text, which I'm going through right now. I had no idea what Carney complex was nor had I even realized that's what was on my 2CK until I encountered it in the JH book (which is residency level).
 
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Phloston said:
11) Cerebriform nuclei; infection with icosahedral, enveloped RNA virus that replicates in the nucleus = ?

11 can also be Sezary syndrome
Click to expand...
Mycosis fungoides/ Sézary’s syndromeis are cutaneous T cell lymphomas.
Not aware of the infection with icosahedral, enveloped RNA virus that replicates in the nucleus in these. What am I missing here ?
 
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Transposony said:
Mycosis fungoides/ Sézary’s syndromeis are cutaneous T cell lymphomas.
Not aware of the infection with icosahedral, enveloped RNA virus that replicates in the nucleus in these. What am I missing here ?
Click to expand...

RNA virus here refers to retroviridae, which is either HIV or HTLV. In this case --> HTLV.
 
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Phloston said:
RNA virus here refers to retroviridae, which is either HIV or HTLV. In this case --> HTLV.
Click to expand...
But isn't HTLV associated with Adult T-cell leukemia/lymphoma and has nothing to do with Mycosis fungoides/ Sézary’s syndrome ?
 
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Transposony said:
But isn't HTLV associated with Adult T-cell leukemia/lymphoma and has nothing to do with Mycosis fungoides/ Sézary’s syndrome ?
Click to expand...

MF/Sezary is a cutaneous T-cell lymphoma/leukemia, respectively, usually caused by HTLV. Late-stage MF (Sezary) usually has the cerebriform cells throughout the bloodstream.
 
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FYI Carney complex is in Robbins and was covered in our cardio and repro classes. It's related to a couple/few concepts that I consider relatively high yield (prolactinomas and papillary thyroid carcinoma):

1. The gene mutation (PRKAR1alpha) is associated with prolactinomas (and GH adenomas)
2. Carney is also associated with the RET/PTC fusion gene, which is commonly found in papillary thyroid carcinomas.

@Phloston glad you mentioned sezary. I thought you were trying to "trick us" with cerebriform nuclei. In Pathoma the cerebriform thing is mentioned as part of sezary syndrome vs mycosis fungoides and I think some people assume "cerebriform nuclei" indicates sezary ONLY. As far as I know, without mention of spread into the blood the dx is mycosis fungoides (right?)

Phloston said:
Nice. Yeah, the mediastinal mass in T-cell leukemia (thymic infiltration) can cause SVC-like syndrome. That's HY on Step 1. Cuz most of the time it's B-cell, but that doesn't have the SVC-like syndrome.
Click to expand...

Is the "red face" thing a pretty classic sign of SVC syndrome-like presentation? I was thinking B-ALL just based on the age of the patient (and "red face" being unrelated).
 
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can anterior spinal artery occlusion causes medial lamniscus damage and result in contralateral loss of tactile discrimination, sense of position and vibration ????
 
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seminoma said:
FYI Carney complex is in Robbins and was covered in our cardio and repro classes. It's related to a couple/few concepts that I consider relatively high yield (prolactinomas and papillary thyroid carcinoma):

1. The gene mutation (PRKAR1alpha) is associated with prolactinomas (and GH adenomas)
2. Carney is also associated with the RET/PTC fusion gene, which is commonly found in papillary thyroid carcinomas.

@Phloston glad you mentioned sezary. I thought you were trying to "trick us" with cerebriform nuclei. In Pathoma the cerebriform thing is mentioned as part of sezary syndrome vs mycosis fungoides and I think some people assume "cerebriform nuclei" indicates sezary ONLY. As far as I know, without mention of spread into the blood the dx is mycosis fungoides (right?)



Is the "red face" thing a pretty classic sign of SVC syndrome-like presentation? I was thinking B-ALL just based on the age of the patient (and "red face" being unrelated).
Click to expand...

For some reason I wasn't notified of you tagging me to this post; I just happened to have seen it randomly.

1) Never heard of that. But acromegaly is a cause of hyperprolactinaemia (since they're often secreted together, and are both JAK/STAT).

2) The question regarding Carney on my 2CK was answerable based on inference alone, but if you knew what it was the question would have made a lot more sense.

3) As far as I'm aware, cerebriform patterning is seen in both MF and SS. Sezary is just advanced MF. Both are caused by HTLV and have similar histology, so they're clearly tied together.

4) Leukemia in a kid (ALL) is most of the time B cell (like 80%). The only time you'd answer T cell as the answer is if there's suggestion of a mediastinal mass (thymic infiltration by leukemic cells). Either they'd mention the mass directly or give you an SVC-like syndrome finding.
 
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From original post:

Name the cancer per the histology:

1) Fallopian-tube like epithelium; benign; female = ?
2) Bilateral, contains psammoma bodies = ?
3) Has intestine-like epithelium; loculated; female = ?
4) Papillary structures with fibrovascular cores; contains psammoma bodies = ?
5) Rows / distinct linearity of cells, bilateral = ?
6) Ataxia, dysarthria, nystagmus, oculomotor dysfunction, muscle rigidity in smoker with recent T2DM = ?
7) Varicocele in 60-year-old smoker = ?
8) I/VI holosystolic murmur at 2nd L-intercostal space in patient with ruddy appearance = ?
9) Perioral melanosis, palpitations, galactorrhea, echocardiography shows L-atrial mass = ?
10) Islands and nests of basophilic cells = ?
11) Cerebriform nuclei; infection with icosahedral, enveloped RNA virus that replicates in the nucleus = ?
12) 5-year-old boy; red face; leukocytosis = ?
13) Fever, bone pain, small blue cells = ?

--------------------

1) Serous cystadenoma of ovary
2) Serous cystadenocarcinoma of ovary
3) Mucinous cystadenoma of ovary
4) Papillary carcinoma of thyroid
5) Lobular carcinoma of breast
6) Small cell lung cancer causing cerebellar dysfunction (anti-Yo antibodies). Anti-Hu are also HY for SCLC but cause encephalomyelitis (asymmetric paresthesias usually) and limbic encephalitis (cognitive dysfunction and personality/emotional changes). SCLC also causes stiff-man syndrome (rigidity of muscles), but that's anti-amphiphysin. In short: just be aware anti-Yo and anti-Hu are SCLC and cause neurological issues.
7) Left-sided RCC, likely clear cell.
8) Carcinoid tumor metastasized to at least the liver
9) Carney complex associated with cardiac rhabdomyoma. These tumors are (higher yield for Step 1) seen in tuberous sclerosis.
10) BCC
11) Mycosis fungoides and/or Sezary syndrome
12) T-cell ALL (mediastinal mass causing SVC-like syndrome; if no mediastinal mass or SVC-like syndrome, leukemia in child is always [on Step 1] B-cell ALL)
13) Ewing sarcoma; often presents like osteomyelitis (hence the fever and bone pain; but be on the lookout for small blue cells, onion skinning or the t11;22, which will tell you it's Ewing)
 
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Is there a difference between good ol' textbook internuclear ophthalmoplegia and the ophthalmoplegia seen in Wernicke's encephalopathy?
 
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A patient takes a large amount of aspirin and is brought to the ED a few hours later. What would be the pH, Bicarb, and PCO2?
 
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Lafakads said:
A patient takes a large amount of aspirin and is brought to the ED a few hours later. What would be the pH, Bicarb, and PCO2?
Click to expand...
Increasing absorption of the salicylic acid causes metabolic acidosis further exacerbated by poisoning of mitochondrial oxidative phosphorylation leading to anaerobic glycolysis and lactic acidosis.
ph decrease
pco2 normal
hco3 decrease
 
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faisal 2000 said:
Increasing absorption of the salicylic acid causes metabolic acidosis further exacerbated by poisoning of mitochondrial oxidative phosphorylation leading to anaerobic glycolysis and lactic acidosis.
ph decrease
pco2 normal
hco3 decrease
Click to expand...
Also causes respiratory alkalosis which is early sign I believe. Late sign is mixed.
pH decrease
pCO2 decrease
HCO3 decrease
 
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Lafakads said:
A patient takes a large amount of aspirin and is brought to the ED a few hours later. What would be the pH, Bicarb, and PCO2?
Click to expand...

"Few hours" needs to be clarified I think. Initial change is respiratory alkalosis, but within 4-24 hours (I think as soon as 4 hrs?) you can see the metabolic acidosis.
 
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Hopefully you guys can help me interpret this question.

Acute occlusion of the common bile duct would lead to?

A. colicky pain + conjugated hyperbilirubinemia
B. colicky pain + no jaundice

I chose "no jaundice" because I figured it would take a little while for the hyperbilirubinemia/jaundice to develop (i.e. the liver doesn't immediately start to spill BDG everywhere). The correct answer was "conjugated hyperbili" though...
 
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seminoma said:
Hopefully you guys can help me interpret this question.

Acute occlusion of the common bile duct would lead to?

A. colicky pain + conjugated hyperbilirubinemia
B. colicky pain + no jaundice

I chose "no jaundice" because I figured it would take a little while for the hyperbilirubinemia/jaundice to develop (i.e. the liver doesn't immediately start to spill BDG everywhere). The correct answer was "conjugated hyperbili" though...
Click to expand...
Where is this from. Also what's the time frame for "acute"?
 
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dfib slim said:
Where is this from. Also what's the time frame for "acute"?
Click to expand...

Kaplan qbank. No time frame given. It was just an ERCP with arrows pointing at the common bile duct and question was something like "acute obstruction of this structure would most likely result in which of the following?" Something like 70% of people got it right though.. which makes me wonder if I'm the only one who misinterpreted what the question was asking.
 
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seminoma said:
Kaplan qbank. No time frame given. It was just an ERCP with arrows pointing at the common bile duct and question was something like "acute obstruction of this structure would most likely result in which of the following?" Something like 70% of people got it right though.. which makes me wonder if I'm the only one who misinterpreted what the question was asking.
Click to expand...
AFAIK "acute" means the onset of symptoms and NOT duration of symptoms.
So, it's typical Kaplan WTF questions where there will be conjugated hyperbilirubinemia but no jaundice initially.
If the arrow was pointing to cystic duct then, of course, there will be no conjugated hyperbilirubinemia.
 
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Transposony said:
oops,,,,No idea
Note to self: Read the question properly.
Click to expand...
Osteopetrosis is a result from defective carbonic anhydrase II --> osteoclasts can't make acid to resorb bone --> excess bone formation by osteoblasts. Since no carbonic anhydrase, you get a mixed proximal (type II) and distal (type I) RTA. Also called RTA type III.
 
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Phloston said:
3) As far as I'm aware, cerebriform patterning is seen in both MF and SS. Sezary is just advanced MF. Both are caused by HTLV and have similar histology, so they're clearly tied together.
Click to expand...
@Phloston
Not sure from where you are getting that both MF and SS are caused by HTLV?
Medscape, UptoDate as well as Robbins & Harrison's don't mention a clear causality.

http://emedicine.medscape.com/article/2139720-overview#aw2aab6b2b3

http://www.uptodate.com/contents/cl...iagnosis-of-mycosis-fungoides?source=see_link
The cause of MF is unclear. Current hypotheses include genetic and epigenetic abnormalities [5-9]. Although environmental and occupational exposure to solvents and chemicals has been implicated in the etiology of the disease, a large case-controlled study failed to support this hypothesis [10]. An infectious etiology for MF has been suggested, but no relation has been confirmed [11]. Human T-lymphotropic virus type I (HTLV-I) has been reported in the peripheral blood or cutaneous lesions of some patients with MF [12,13]. However, an equal number of studies have evidence against a role of HTLV-I [14,15].
Click to expand...
 
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dfib slim said:
I know is causes a hyperchloremic metabolic acidosis but never thought about why. Just assumed it had something to do with bicarb and chloride liking to switch places.
Click to expand...
Correct.
Chloride is excreted as Ammonium Chloride. For this to happen, Ammonia is protonated to Ammonium. Since H+ is no longer secreted by the intercalated cells in RTAs, the Cl- cannot be excreted and reabsorbed to maintain electroneutrality.
 
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aspiringmd1015 said:
In MS, are the axons preserved or destroyed? kaplan q bank states the axons are preserved, FA says theyre destroyed
Click to expand...

yeah i was too really confused when i came across that and after looking it up from multiple sources this is what i have come to conclusion.

there is definitely demyelination of Axon called denudation( there is no neuronal loss or AXONAL disruption), only the outer covering is been removed----> depletion of oligodendrocyte( myelin producing cell as they try to make myelin which is been lost)---> microglial/ macrophage(due to damage to BBB) move to the area and phagocytose the products of myelin breakdown----> as in with any CNS injury--> astrocyte move in ---> fibrillary astrocytosis---> glial scar= Sclerosis.

hence the name multiple sclerosis.
This process is what makes the diagnostic finding on MRI: Periventricular plaque = which are made from reactive gloss + loss of oligodendrocyte.


and also keep in mind its this lost of demyelination---> slower conduction---> slow visual evoked potential.
 
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Phloston said:
HTLV infection is definitely associated with MF and SS.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC295510/

That's just one article.
Click to expand...
@Phloston
That's a 20 years old article.

Correct me if I am wrong but since then MF and SS have been proven not to be associated with HTLV as early as 1997.
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.1997.3213138.x/epdf

I was wondering why none of the latest textbooks and recent article don't even consider HTLV as a causative agent anymore.
I found the answer from a review article in NEJM in 2004.
http://www.nejm.org/doi/full/10.1056/NEJMra032810

Some recent articles about pathogenesis:
http://www.ncbi.nlm.nih.gov/pubmed/24438969
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699909/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278552/

Here are some latest 2015 review articles:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374776/
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2011.08852.x/full
 
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Transposony said:
@Phloston
That's a 20 years old article.

Correct me if I am wrong but since then MF and SS have been proven not to be associated with HTLV as early as 1997.
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.1997.3213138.x/epdf

I was wondering why none of the latest textbooks and recent article don't even consider HTLV as a causative agent anymore.
I found the answer from a review article in NEJM in 2004.
http://www.nejm.org/doi/full/10.1056/NEJMra032810

Some recent articles about pathogenesis:
http://www.ncbi.nlm.nih.gov/pubmed/24438969
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699909/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278552/

Here are some latest 2015 review articles:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374776/
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2011.08852.x/full
Click to expand...

I've been through the research process and the only thing it's made me is more cynical and dismissive of new research (which is unfortunate). It's articles like this that are the reason: http://www.ncbi.nlm.nih.gov/pubmed/9326191

It bases its conclusion off of studies of people with MF/SS, where it found lack of HTLV RNA on PCR. In reality, the only conclusion they instead should make is: Mycosis fungoides and Sezary syndrome need not be caused by HTLV. That's let alone the fact that none of their subjects are from Japan, which is where HTLV prevalence is high.

I just wouldn't go around saying MF and SS are not associated with HTLV.

We know HTLV causes T-cell lymphoma/leukemia.

MF/SS are T-cell lymphoma/leukemia (the latter a progression).

Does everyone with T-cell lymphoma/leukemia need to have HTLV infection? No. But if you took the world's population that has been infected with HTLV, you will see MF/SS in a portion of them.

There's reasonable causality.
 
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lmao, atp7b is mutated in wilsons, so i thought maybe atp7b was only in the canalicular protein, while atp7a is found in your entire body, mostly your gut for copper absorption
 
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