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

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Transposony said:
A 55 year-old female presents with difficult and painful swallowing, a swollen red tongue and inflammation at the corners of her mouth. Endoscopy of her esophagus reveals the presence of webs and a biopsy of a lesion in her esophagus is concerning for squamous cell carcinoma. Her peripheral blood smear is most likely to reveal which of the following?
a. Heinz bodies
b. Hypochromic microcytosis
c. Macrocytosis and hypersegmented neutrophils
d. Schistocytes
e. Spherocytes
Click to expand...

Transposony said:
A 50 year-old male with chronic renal failure due to diabetic nephropathy comes to the ER after his family notes that he has been vomiting and confused for the past two days. He has also been complaining of muscle cramps and multiple excoriations are evident on his arms and legs. His family admits that he has missed his last several dialysis appointments because he said that "he didn't like the way they felt". On physical exam, his doctor notes that the patient's neck veins bulge when he is breathing in. This is most likely due to:
a. Increased blood viscosity
b. Inflammation of the pericardium
c. Neurological toxicity
d. Pulmonary embolism
e. Volume overload
Click to expand...

Transposony said:
A six-month old girl is brought to her new pediatrician with a three-day history of fever. A review of her medical history reveals a consistently high WBC count and delayed umbilical cord separation. Her history is also significant for an infection of her umbilical cord stump with Staphylococcus aureus characterized by cellulitis but notably without pus, and her WBC count at the time was markedly elevated (45 X 109/L). Analysis of her WBCs by flow cytometry is shown below. Which of the following pairs of markers was most likely used to determine the nature of this girl's immunodeficiency?

View attachment 196886
Click to expand...

Thanks a lot @Transposony for the explanation.
As for my other question, the questions you posted are they from Becker qbank? I'm thinking of trying it out that's why asking. I liked these questions you posted. Thanks
 
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differentiating features of
median nerve lesion Vs ulnar nerve lesion.
ulnar nerve lesion Vs dupetryne contracture

what is ulnar paradox
 
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faisal 2000 said:
why ACEI contrindicated in renal artery stenosis ? [/USER]
Click to expand...

In renal artery stenosis the renal perfusion pressure is low (afferent arteriole is not getting enough blood).
Angiotensin II maintains the glomerular pressure (and, therefore, GFR) by constricting the efferent arteriole.
Inhibition of ACE can, therefore, induce acute renal insufficiency in patients with bilateral renal artery stenosis.
 
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Hey guys, new sdn member here, can anyone recommend a concise neuroanatomy source for step 1 purposes?

this thread is golden btw.

Thanks!
 
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Job's syndrome (Hyper-IgE Syndrome):

According to FA15: is a T-cell disorder, defect is in Th17 cells
According to kaplan: is a phagocyte dysfunction, Th1 cells cannot make IFN
According to levinson: is a phagocyte dysfunction, T-helper cells cannot make IFN

I know the end result is that neutrophil chemotaxis doesn't work properly & phagocytosis is affected. But if we talk about the mechanism behind it, which one of the above is correct?

If someone can please clarify.
Thanks a bunch
 
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Reperfused said:
Job's syndrome (Hyper-IgE Syndrome):

According to FA15: is a T-cell disorder, defect is in Th17 cells
According to kaplan: is a phagocyte dysfunction, Th1 cells cannot make IFN
According to levinson: is a phagocyte dysfunction, T-helper cells cannot make IFN

I know the end result is that neutrophil chemotaxis doesn't work properly & phagocytosis is affected. But if we talk about the mechanism behind it, which one of the above is correct?

If someone can please clarify.
Thanks a bunch
Click to expand...

Pulled from Rapid Review Pathology: "Job syndrome is AD (sometimes recessive) disorder of neutrophils. Most patients have unaffected parents. It is due to a mutation in STAT 3, whose protein products act as transcription activators. There is also a reduction in T17 Helper T cells, which produce IL-17, a chemotactic agent for monocytes and neutrophils. Therefore neutrophils and monocytes in these patients have abnormal chemotaxis, leading to "cold" soft tissue abscesses and recurrent pneumonias."
 
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Gumdrops, thanks for providing your help.
Unfortunately, my question remains unanswered. I quoted 3 resources and I am sure other resources would say sightly different things too.
My question is, which resource is correct?? I completely understand what each of the resource is trying to explain. Understanding the concept isn't a problem so that's not what I am asking. I just wanna know which one to believe for this particular disease?
If someone can give their input.
 
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Reperfused said:
Gumdrops, thanks for providing your help.
Unfortunately, my question remains unanswered. I quoted 3 resources and I am sure other resources would say sightly different things too.
My question is, which resource is correct?? I completely understand what each of the resource is trying to explain. Understanding the concept isn't a problem so that's not what I am asking. I just wanna know which one to believe for this particular disease?
If someone can give their input.
Click to expand...

So I don't think any of what you're saying is entirely correct. Don't want to be rude, just want to save you the time.
Directly from First Aid 2015 on Job Syndrome: "Deficiency of Th17 cells due to Stat3 mutation -> impaired recruitment of neutrophils to sites of infection. Increased IgE, decreased IFN"

Job syndrome is abnormal neutrophil chemotaxis that's due to deficiency in Th17 cells (a type of helper T-cell). The phagocytes are dysfunctional because of the decrease in Th17 cells (not enough IL-17 anymore). The decrease in Th17 is due to the Stat3 mutation. So it all stems from the Stat3 mutation.

Looks like RR and FA are in nice agreement here. Also, it says nothing in FA or RR about the helper T-cells not being able to make enough IFN. IFN decrease is seen in Job syndrome but I'm not sure that Th1 cells being unable to produce IFN is the reason why. Can you directly cite a source that says this? Your paraphrase of FA leads me to believe that the problem is with interpretation rather than disagreeing sources.
 
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I quoted all my sources in my original message. And what I wrote about FA15 saying is the same thing as what you wrote about FA15 saying (you might wanna read my original message again).
 
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Reperfused said:
I quoted all my sources in my original message. And what I wrote about FA15 saying is the same thing as what you wrote about FA15 saying (you might wanna read my original message again).
Click to expand...

We didn't write the same thing at all. Also, anyone can go to FA 2015, look up Job Syndrome and see that you didn't quote FA 2015 either. Best of luck to you.
 
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I had no intentions of starting an argument here but please stop trying to prove that I wrote wrong stuff, because I didn't.
Your failure to see that I did mention sources for all the phrases I quoted, and asking me to cite a source, leads me to believe that you misread my original message.

Reperfused said:
Job's syndrome (Hyper-IgE Syndrome):

According to FA15: is a T-cell disorder, defect is in Th17 cells
According to kaplan: is a phagocyte dysfunction, Th1 cells cannot make IFN
According to levinson: is a phagocyte dysfunction, T-helper cells cannot make IFN

I know the end result is that neutrophil chemotaxis doesn't work properly & phagocytosis is affected. But if we talk about the mechanism behind it, which one of the above is correct?

If someone can please clarify.
Thanks a bunch
Click to expand...

Please let me know what did I write here that's not written in FA15?
Seriously, anyone can open all the 3 books and check.
 
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which disease can cause chest pain with dysphagia for solids and liquids ?? i am thinking about hiatal hernia but i am not sure
 
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@faisal 2000 that looks like Diffuse Esophageal Spasm --> May resemble MI , do EKG to rule out and give a CCB or something to relax the smooth muscle
 
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I'm going through UWorld for Step 3 right now and they've asked TWO questions on this so far on C. difficile Tx in the first third of the QBank I've done:

If WBC count <15,000 AND creatinine <1.5x baseline AND serum protein >2.5 g/dL = mild pseudomembranous colitis; Tx = oral metronidazole

If outside those parameters above = severe pseudomembranous colitis; Tx = oral vancomycin, NOT oral metronidazole

If ileus is present (which is severe), Tx = oral vancomycin + IV metronidazole, OR rectal vancomycin

If those treatments are refractory, then surgery (i.e., subtotal colectomy or diverting loop ileostomy with colonic lavage) may be indicated.

They also want you to know that if you give oral metro for mild illness and it doesn't work, the next best step is giving oral metro again. The first recurrence is Tx with oral metro again if mild or oral vanc if severe. This is because it's thought most first recurrences are due to germination of spores from the initial infection rather than a genuine second infection.

The second recurrence is treated with pulsed tapering of oral vancomycin for 6-7 weeks.

Subsequent recurrences are treated with fidaxomicin.


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

On Step 1, the answer for this question as far as I had previously been aware was always oral metronidazole before oral vancomycin based on wanting to decrease resistance risk. I doubt at the Step 1 level they'd be nitpicky about the severity of it and want you to know most cases are treated first with oral metro. But UW Step 3 had a question with severe pseudomembranous, and most DOCTORS chose oral metro but it was oral vanc to start.
 
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Reperfused said:
Gumdrops, thanks for providing your help.
Unfortunately, my question remains unanswered. I quoted 3 resources and I am sure other resources would say sightly different things too.
My question is, which resource is correct?? I completely understand what each of the resource is trying to explain. Understanding the concept isn't a problem so that's not what I am asking. I just wanna know which one to believe for this particular disease?
If someone can give their input.
Click to expand...

I dont know if its still relevant but i d like to contribute coz I think I remember about this from a lecture

To my understanding --> Impaired monocyte chemotaxis to immune stimulus site ---> No monocytes to turn to macrophages --> No CD4-Th1 / Macrophage interaction ---> Reduced Th1 response cytokines ( IFN - γ , Tnf , etc etc ) --> Immune responses shift towards Th2 --> Increased Ig-E , minor increase in Ig-A
 
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faisal 2000 said:
how does TGF-β play important role in Idiopathic pulmonary fibrosis ?
what is the mechanism (by details) beyond cellular injury in iron toxicity ?

Click to expand...

1- TGF-β1 decreases caveolin-1 which is a protein that inhibits fibrosis.
2- Excessive iron can overwhelm the body’s ability to bind the absorbed free iron with the transport protein transferrin. The free iron contributes to generation of cellular free radicals via the Fenton reaction.
 
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faisal 2000 said:
how vitamin K and vitamin B12 deficiencies cause abdominal pain ?



@Phloston
Click to expand...

Can't say I've heard of these two vitamins directly causing abdominal pain. My assumption would be things unrelated (e.g., IBS, primary dysmenorrhea) or tangentially related (e.g., pernicious anaemia with indigestion, or floral imbalances with increases susceptibility to malabsorption/indigestion, or bleeding tendencies). Perhaps someone could post an article that digs something up, but as I said, I've never heard of those vitamins causing abdominal pain directly.
 
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faisal 2000 said:
for step1 , what should i know about HCM, DCM, RCM ?
@Transposony@Phloston
Click to expand...
FA is sufficient and I would know that HCM murmur (as well as MVP) does not follow the rule of more blood, more murmur.
Pompe disease, Sudden cardiac death are associated with Hypertrophic cardiomyopathy.
Also, dilated cardiomyopathy is more commonly associated with hemochromatosis than RCM.
 
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Transposony said:
FA is sufficient and I would know that HCM murmur (as well as MVP) does not follow the rule of more blood, more murmur.
Pompe disease, Sudden cardiac death are associated with Hypertrophic cardiomyopathy.
Also, dilated cardiomyopathy is more commonly associated with hemochromatosis than RCM.
Click to expand...
what about fabry's disease is it associated mainly with RCM or HCM ?
how does hemochromatosis cause RCM ?
 
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faisal 2000 said:
what about fabry's disease is it associated mainly with RCM or HCM ?
how does hemochromatosis cause RCM ?
Click to expand...
I don't think you need to know the type of hypertrophy in Fabry disease for Step 1 since there are no specific type of hypertrophy but just left ventricular hypertrophy.
What you should know that it frequently presents as stroke and most of it's effects are due to deposition of glycosphingolipids in epithelial, smooth muscle cells and in the blood vessels of various organs eventually leading to ischemia and organ damage.

For hemochromatosis > free radicals (Fenton reaction) --> myocardial damage --> Fibrosis
 
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Transposony said:
I don't think you need to know the type of hypertrophy in Fabry disease for Step 1 since there are no specific type of hypertrophy but just left ventricular hypertrophy.
What you should know that it frequently presents as stroke and most of it's effects are due to deposition of glycosphingolipids in epithelial, smooth muscle cells and in the blood vessels of various organs eventually leading to ischemia and organ damage.

For hemochromatosis > free radicals (Fenton reaction) --> myocardial damage --> Fibrosis
Click to expand...
i meant how hemochromatosis cause DCM ?
 
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faisal 2000 said:
i meant how hemochromatosis cause DCM ?
Click to expand...
Same mechanism.
Myocardial damage can either lead to DCM or RCM depending on the extent and duration of injury from iron and the body's response to such insult and the time to diagnosis (i.e. presentation).
For Step 1 purposes DCM is more common than RCM.
 
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faisal 2000 said:
why there is hyperlipdemia and hyponatremia in hypothyroidism ??
also hypothyroidism causes HTN due to fluid retention what is the mechanism behind that?



@Transposony @Phloston
Click to expand...
As far as what I can recall thyroid hormones upregulate Na/K ATPase pumps, so lower hormone levels keep more sodium in the cells vs plasma, or even in urine vs tubular cells. Beta agonism has a similar effect (indirect) as thyroid hormone I believe because of peripheral conversion (and propranolol is best to inhibit that).
 
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1. Cyclosporine uses: Prevent transplant rejection, psoriasis, and severe RA. Why would you use it for RA when RA is a type 3 HS rxn and cyclosporine inhibits calcineurin which inhibits IL-2 which would inhibit T-cells? (since RA isn't a type 4 HS)

2. If you have a patient that had a transplant and was on immunosuppressants for 2 years, but then stopped the immunosuppressant and had a reaction after stopping, what kind of rejection would this be? It has been over 2 years but I think chronic is specifically if she is on the medication and gets a reaction months-years later (while still on the rx) so not this one? Not sure about acute vs hyper acute in this situation. Would it be hyper acute if they specified the rxn occurred minutes - hours in this situation? or would it just be acute in general bc that's what you give immunosuppressants for especially? Thanks!


@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma
 
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tvelocity514 said:
1. Cyclosporine uses: Prevent transplant rejection, psoriasis, and severe RA. Why would you use it for RA when RA is a type 3 HS rxn and cyclosporine inhibits calcineurin which inhibits IL-2 which would inhibit T-cells? (since RA isn't a type 4 HS)

2. If you have a patient that had a transplant and was on immunosuppressants for 2 years, but then stopped the immunosuppressant and had a reaction after stopping, what kind of rejection would this be? It has been over 2 years but I think chronic is specifically if she is on the medication and gets a reaction months-years later (while still on the rx) so not this one? Not sure about acute vs hyper acute in this situation. Would it be hyper acute if they specified the rxn occurred minutes - hours in this situation? or would it just be acute in general bc that's what you give immunosuppressants for especially? Thanks!
Click to expand...

1. T-cells are involved in antibody productions (Th2). So, if you block Th2 cells then you also block antibody production.
This is the most simplified mechanism but there are many more mechanisms involved since IL2 has many functions.

2. Hyperacute rejection is due to pre-formed antibodies so it only happens at the time of transplantation i.e. on the operating table when the surgeon opens the vascular clamp to perfuse the newly transplanted kidney. It cannot happen later on and there is no treatment but only prevention by accurate cross-matching.

When the patient stops the immunosuppressants after 2 years then they will get acute rejection since those immunosuppressants are no longer blocking the T cells.

Chronic rejection (aka Chronic Graft Nephropathy) is due to many causes including graft ischemia, re-perfusion injury, concentric intimal thickening , immunosuppressant toxicity, multiple treated acute rejection episodes etc. All this leads to progressive fibrosis and tissue remodeling --> multilayering of the peritubular capillaries, interstitial fibrosis, and tubular atrophy.
Hope this helps.
 
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tvelocity514 said:
1. Cyclosporine uses: Prevent transplant rejection, psoriasis, and severe RA. Why would you use it for RA when RA is a type 3 HS rxn and cyclosporine inhibits calcineurin which inhibits IL-2 which would inhibit T-cells? (since RA isn't a type 4 HS)

2. If you have a patient that had a transplant and was on immunosuppressants for 2 years, but then stopped the immunosuppressant and had a reaction after stopping, what kind of rejection would this be? It has been over 2 years but I think chronic is specifically if she is on the medication and gets a reaction months-years later (while still on the rx) so not this one? Not sure about acute vs hyper acute in this situation. Would it be hyper acute if they specified the rxn occurred minutes - hours in this situation? or would it just be acute in general bc that's what you give immunosuppressants for especially? Thanks!


@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma
Click to expand...

There is a type 4 HS component in RA. The joint damage = type 4HS.
 
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Which E. coli affects the ADP ribosylation of G-proteins? I feel like it's ETEC (bc it increases cAMP) - but if so, I'm surprised that bacillus anthracis was not added to this list . (diphtheria, pseudomonas, cholera, e. coli, pertussis).

If it is ETEC, what G-protein is it?

Thanks!

@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma
 
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doesnt ETEC like have 2 toxins?? Stable on the Ground ST-Gcmp
Labile on the Air LT-Camp

Probably both adp ribosylate the stuff that makes cAMP , and gCMP to work all the time..

As far as I remember its the a Gs subunit that activates adenylate/guanylate cyclase
 
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tvelocity514 said:
Which E. coli affects the ADP ribosylation of G-proteins? I feel like it's ETEC (bc it increases cAMP) - but if so, I'm surprised that bacillus anthracis was not added to this list . (diphtheria, pseudomonas, cholera, e. coli, pertussis).

If it is ETEC, what G-protein is it?
Click to expand...
@tvelocity514

EF-1 and EF-2 are G-Proteins just like Gs, G1 and Gq and derive energy from GTP but unlike them they are only involved in protein synthesis and do not take part in signal transduction.

ADP-ribose covalently binds alpha -subunit of G-proteins inactivating or activating it depending on the exotoxin.

Diphtheria & Pseudomonas toxins ADP-ribosylate EF-2 inactivating it → inhibition of protein synthesis.

Cholera & E.coli (ETEC) toxins ADP-ribosylate Gs activating it (stimulates the stimulator) → turns on adenylate cyclase → increases cAMP
.
Pertussis toxin ADP-ribosylates Gi and inactivates it (inhibits the inhibitor) → turns on adenylate cyclase → increases cAMP

Bacillus anthracis (edema factor) toxin itself acts as an adenylate cyclase. There is no G-protein involved and that's why it doesn't belong to the list.

Shiga toxin and EHEC (aka verotoxin, Shiga-like toxin) acts like a glycosylase which cleaves adenine residue from 28S subunit of r-RNA → prevents EF-1 to attach the t-RNA binding to A-site → inhibition of protein synthesis.
 
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faisal 2000 said:
why ACEI contrindicated in renal artery stenosis ?
Click to expand...
Remember that renal artery stenosis induces secondary hyperaldosteronism due to reduced blood flow. Therefore, a single dose of ACEI (captopril) will abruptly reduce renal function in the already ischemic kidney
 
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Mom goes to ER with 4 month old daughter. Kid is dehydrated, lethargic. Mom says baby has not been feeding well for the past few days. Mother said she changed the baby's bottle to cow's milk because kids did not like the taste of the formula. What is in the cow milk that could cause these symptoms?
1-Linoleic acid
2-Linolenic acid
3-Calcium
4-Protein

@Phloston
@Transposony
 
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I can never remember Sturge-Weber vs Von hippel-Lindau vs Tuberous Sclerosis vs Osler-Weber-Rendu syndrome. I'm pretty sure OWR doesnt even belong in the group with the other 3. How do you keep these weird diseases straight in your mind?
 
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chillaxbro said:
I can never remember Sturge-Weber vs Von hippel-Lindau vs Tuberous Sclerosis vs Osler-Weber-Rendu syndrome. I'm pretty sure OWR doesnt even belong in the group with the other 3. How do you keep these weird diseases straight in your mind?
Click to expand...
Sturge-Weber: AV malformations of the face (trigeminal nerve distribution) and brain.
Tuberous Sclerosis: hypopigmented skin lesions ("ash leaf spots") and brain hamartomas, rhabdomyomas/heart tumers at a young age.
VHL: Bilateral Renal Cell Carcinoma and Pheos
 
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