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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dfib slim said:
Which IBD are they more associated with?
Click to expand...
i think this more helpful : serum antibacterial antibodies are present in patients with ulcerative colitis, they are much more common and are found in higher titers in patients with Crohn's disease. Furthermore, the range of antibodies against bacterial antigens (anti-I2, anti-OmpC, and anti-CBir1 antibodies) and fungal antigens (anti–Saccharomyces cerevisiae antibodies [ASCA] is broader in Crohn's disease, whereas the only ulcerative colitis–
associated antibody is perinuclear antineutrophil cytoplasmic antibody (pANCA), which recognizes nuclear antigens that may cross-react with bacterial antigens.
 
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faisal 2000 said:
i think this more helpful : serum antibacterial antibodies are present in patients with ulcerative colitis, they are much more common and are found in higher titers in patients with Crohn's disease. Furthermore, the range of antibodies against bacterial antigens (anti-I2, anti-OmpC, and anti-CBir1 antibodies) and fungal antigens (anti–Saccharomyces cerevisiae antibodies [ASCA] is broader in Crohn's disease, whereas the only ulcerative colitis–
associated antibody is perinuclear antineutrophil cytoplasmic antibody (pANCA), which recognizes nuclear antigens that may cross-react with bacterial antigens.
Click to expand...
What I was getting at was ASCA is more associated with Crohn's and pANCA with UC. I wasn't asking for help, just adding to the concept thread.
 
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guys as i know anti sac fount in step2 books master the board ? is that conept tested in step1? as i didnt found this info in nbme or uworld or kaplan q bank and rx or pathoma
 
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syoung said:
salmonella (atypical) > staph aureus
Click to expand...

Idk, I'm pretty sure Sattar says staph is still more common than salmonella (even though the association is salmonella).

If I remember correctly the actual epidemiology is salmonella in sickle cell >>> general population; in general population s.aureus>>>>salmonella, and in sickle cell population s.aureus > salmonella. Could be wrong.. but either way on a test I will always pick salmonella in the context of sickle cell unless there's something in the stem that oints to s.aureus (like culture/stain)
 
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seminoma said:
Idk, I'm pretty sure Sattar says staph is still more common than salmonella (even though the association is salmonella).

If I remember correctly the actual epidemiology is salmonella in sickle cell >>> general population; in general population s.aureus>>>>salmonella, and in sickle cell population s.aureus > salmonella. Could be wrong.. but either way on a test I will always pick salmonella in the context of sickle cell unless there's something in the stem that oints to s.aureus (like culture/stain)
Click to expand...
Goljan has Salmonella as the MMC of osteomyelitis in SSD. I also found these sources.

http://www.aafp.org/afp/2000/0915/p1309.html#afp20000915p1309-b5

http://pediatrics.aappublications.org/content/101/2/296.extract

http://www.sciencedirect.com/science/article/pii/S1201971209001453

http://pubs.rsna.org/doi/full/10.1148/radiographics.21.4.g01jl23971
 
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Firecracker describes Chlamydophila pneumoniae presenting with "Chest X-ray usually shows one patchy area of subsegmental infiltration" vs. C. psittaci as lobar pneumonia
When they say "subsegmental" do they actually mean interstitial?
 
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TheBunkMD said:
Firecracker describes Chlamydophila pneumoniae presenting with "Chest X-ray usually shows one patchy area of subsegmental infiltration" vs. C. psittaci as lobar pneumonia
When they say "subsegmental" do they actually mean interstitial?
Click to expand...

Segmental bronchi supply a bronchopulmonary segment (10 in the right lung, 8 in the left). Subsegmental bronchi are the branches off of a segmental bronchi and supply an even smaller area within each lung. So, a subsegmental infiltrate is infiltration of a smaller area than a lobe or a bronchopulmonary segment. I believe it can be either interstitial or intraalveolar despite a lot of us being taught that atypical organisms cause "interstitial" pneumonia.
 
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seminoma said:
Thanks. Hopefully I'll learn this when we do GI..
Click to expand...
It's more of a Step 2 CK material since I only came across it while preparing for CK.
Just like antibodies against neutrophils (pANCA) these are antibodies against the yeast Saccharomyces cerevisiae (ASCA).
Saccharomyces cerevisiae is the common yeast used in baking ("baker's yeast") and brewing ("brewer's yeast") in food industry. The major pathological concept in CD is the loss of immune tolerance towards the resident flora. Antibodies against this yeast are present in patients with IBD and their serum levels are useful in the differentiating CD from UC.
 
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Transposony said:
It's more of a Step 2 CK material since I only came across it while preparing for CK.
Just like antibodies against neutrophils (pANCA) these are antibodies against the yeast Saccharomyces cerevisiae (ASCA).
Saccharomyces cerevisiae is the common yeast used in baking ("baker's yeast") and brewing ("brewer's yeast") in food industry. The major pathological concept in CD is the loss of immune tolerance towards the resident flora. Antibodies against this yeast are present in patients with IBD and their serum levels are useful in the differentiating CD from UC.
Click to expand...

Good **** (pun intended).
 
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dfib slim said:
Anticholenergics for EPS but by the time it gets to tardive dyskinesia it's irreversible correct?
Click to expand...
i think we should switch to atypical antipsychotic drugs(e.g.,Clozapine,Risperidone) because they can minimize tradive dyskinesia but if these drugs do not work we can use benzotropine
 
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KAM25 said:
How can one differentiate between an osteoblastic mets and a lytic mets on xray?
Click to expand...
Osteoblast-->bone forming (Sclerotic-->appears whitish on Xray) v/s Osteoclast-->bone destroying (lytic-->appears dark holes on Xray).
 
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side effects of antipsychotic drugs :

Parkinsonism like syndrome --> treated by decreasing the dose of neuroleptic and give benztropine.
Akathesia: motor restlessness --> treated by benzodiazepines, anticholinergic agent, or propranolol
Dystonia: muscle spasm (involunry movements, retlessness, Protuding tounge, fixed upward gaze, Torticolis (Involuntry spasm of neck muscles)Dopaminergic Sites:at Nigrostriatal Sites
dystonia --> treated by benzodiazepines & anticholinergic agent.

Tardive dyskinesia(choreoathetoid movement of face and tongue due to D-receptors sensitization) --> treated by using atypical antipsychotic instead of the typical antipsychotic drugs.
 
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MOA of diptheria toxin i.e. ADP Ribosylation ?
I mean what is ADP Ribosylation and how and where does it act to bring about the toxin's effect?
 
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Anticoagulant Anti-platelet drug which is ineffective when taken with a CYP2C19 inhibitor ?
 
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seminoma said:
Mechanism of pertussis induced lymphocytosis?
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ADP-ribosylation of lymphocytes ------> messed up intracellualr signalling (revved up cAMP) ------> decreased high endothelial venules extravasation
---------> decreased entry of lymphocytes into lymph nodes ------> lymphocytosis (relative not absolute).
It is quite similar to steroid induced neutrophilia.
 
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Spoiler Alert (UW)
A middle aged woman presents complains about the changes in her body. She says that her legs are getting skinnier and her belly is getting wider. She also complains of always feeling fatigued. Examination shows adipose tissue loss from extremities and gluteal region with increase in abdominal girth. The patients situation is the result of medication. What is she likely being treated for?

a) Thyroid nobule b) Osteoarthritis c) Peptic ulcer disease d) Hypercholesterolemia e) HIV
 
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NoLollipops4U said:
A middle aged woman presents complains about the changes in her body. She says that her legs are getting skinnier and her belly is getting wider. She also complains of always feeling fatigued. Examination shows adipose tissue loss from extremities and gluteal region with increase in abdominal girth. The patients situation is the result of medication. What is she likely being treated for?

a) Thyroid nobule b) Osteoarthritis c) Peptic ulcer disease d) Hypercholesterolemia e) HIV
Click to expand...
HAART-associated lipodystrophy.
 
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23 y/o F patient presents to your ER unconscious. You notice a scar on her neck from prior surgery. Family members tell you that earlier before passing out, her mental status had progressively got worse and she was in a stupor. They mention something about her being treated for some kind of condition where "her immune system was attacking itself." You note she has cold skin, slow heart rate, and her breathing is also very slow.

What condition is this patient presenting with, and what should be your first medical treatment?
 
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NoLollipops4U said:
Yep. Basically a UW question. Most people, including myself, jumped to OA thinking steroids and cushings....not many people got it right. What drug class?!
Click to expand...
Protease inhibitors e.g Indinavir

P.S. Please put a "spoiler alert" on the top if you are posting Qs from NBMEs or three main Q Banks for the people who has not yet done those Q Banks.
 
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pathologyDO said:
23 y/o F patient presents to your ER unconscious. You notice a scar on her neck from prior surgery. Family members tell you that earlier before passing out, her mental status had progressively got worse and she was in a stupor. They mention something about her being treated for some kind of condition where "her immune system was attacking itself." You note she has cold skin, slow heart rate, and her breathing is also very slow.

What condition is this patient presenting with, and what should be your first medical treatment?
Click to expand...
Acute adrenal insufficiency. Hydrocortisone and lots of saline.
Scar on her neck due to thyroidectomy for Hashimoto's thyroiditis.
 
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Transposony said:
Acute adrenal insufficiency. Hydrocortisone and lots of saline.
Click to expand...

This was an example of myxedematous coma characterized by hypothermia, hypocapnia, and you would also see hypothyroid problems like bradycardia. The surgery scars over the neck were from removal of thyroid due to autoimmune disorder and thus presentation of hypothyroidism.

If you run into a patient such as this, you must prophylactic ally treat with hydrocortisone in case this is adrenal insufficiency, even with high suspicion of thyroid pathology.
 
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I need a bit of help understanding the hypocalcemia and hypomagnesemia with loop diuretic use.

The drug blocks the Na/K/Cl symport. So K stays OUT of the cell and remains in the lumen. This should lead to less K inside the cell passively leaking out back into the lumen, thus not creating a positively charged luminal membrane.

Should this not make it easier for Mg2+ and Ca2+ to be reabsorbed back into the blood?
 
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Potassium is shifted so that more of it is outside the cell in the lumen. This means more (+) charge in the lumen, which blocks the paracellular transport of Mg/Ca2+. More sodium is there too which also adds to the positivity. I don't really know why a positive luminal potential would block reabsorption of Mg/Ca2+, just that it happens.

Found this, hope it helps:

screen_shot_2011-09-30_at_12.02.17_am1317355380274.png
 
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Ahhhh ok, thank you!

I don't really know why a positive luminal potential would block reabsorption of Mg/Ca2+, just that it happens.
Click to expand...

Since they are both cations, the positive charges repel.
 
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messengers said:
I need a bit of help understanding the hypocalcemia and hypomagnesemia with loop diuretic use.

The drug blocks the Na/K/Cl symport. So K stays OUT of the cell and remains in the lumen. This should lead to less K inside the cell passively leaking out back into the lumen, thus not creating a positively charged luminal membrane.

Should this not make it easier for Mg2+ and Ca2+ to be reabsorbed back into the blood?
Click to expand...
Normally, there is active reabsorption of Na+, K+, and Cl- by Na+/K+/2Cl– cotransporter at the thick ascending loop of Henle which indirectly induces the paracellular reabsorption of Mg2+ and Ca2+ through (+) lumen potential generated by K+ backleak.
Loop diuretics inhibits Na+/K+/2Cl– cotransporter at the thick ascending loop of Henle. So, no K+ backleak, no paracellular reabsorption of Mg2+ and Ca2+.
 
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Transposony said:
Normally, there is active reabsorption of Na+, K+, and Cl- by Na+/K+/2Cl– cotransporter at the thick ascending loop of Henle which indirectly induces the paracellular reabsorption of Mg2+ and Ca2+ through (+) lumen potential generated by K+ backleak.
Loop diuretics inhibits Na+/K+/2Cl– cotransporter at the thick ascending loop of Henle. So, no K+ backleak, no paracellular reabsorption of Mg2+ and Ca2+.
Click to expand...

So this is what still doesn't add up for me.. the K+ backleak should be leading to a more (+) membrane potential. Yet blocking the Na/K/Cl transporter also makes the lumen membrane potential (+). Is it then the difference in magnitude of positive charge that blocks the paracellular transport? That's all I can come up with to explain it.
 
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pathologyDO said:
So this is what still doesn't add up for me.. the K+ backleak should be leading to a more (+) membrane potential. Yet blocking the Na/K/Cl transporter also makes the lumen membrane potential (+). Is it then the difference in magnitude of positive charge that blocks the paracellular transport? That's all I can come up with to explain it.
Click to expand...

The K+ backleak makes the lumen more positively charged. The Mg2+ and Ca2+ do whatever they can to get away from all the K+ floating around in the lumen. Eventually Mg and Ca find their way to the membrane and escape.

Btw, is that pic you attached from your classnotes? If so, I'm super jealous...
 
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