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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1- clostridium tetani causes upper or lower motor neuron lesion ?
2- what happen if there is damage in lateral striate arteries
 
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Transposony said:
What is the mechanism of aldosterone synthesis?
Click to expand...
cholesterol converted into prgnenolone by desmolase which regulated by ACTH. then pregnenolone go into smooth er and converted into progesterone by 3b hydroxysteroid dehydrogenase. then progesterone undergo hydroxylation at 21c,11, also dehydrogenase at 18c. now become aldosterone.

aldosterone --> hydroxylation at 21c,and 11 .dehydrogenase at 18c
glucocorticoides --> hydroxylation at 21c, 17c,21c, and 11c
testosterone --> hydroxylation at 17 c , 19c. 17, and 20 lyase .
 
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If Aldosterone synthesis is regulated by ACTH then how does renin–angiotensin–aldosterone system works?
 
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Transposony said:
If Aldosterone synthesis is regulated by ACTH then how does renin–angiotensin–aldosterone system works?
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if there is hypotenstion that will causes decrease in renal perfusion pressure which increase renin secretion .
renin-->anigotesin 1 --> angiotensin 2 -->more aldosterone -->more Na reabsorption with water and increase k secretion
 
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more specific^ renin converts alpha angiotensinogen(protein made by the liver to angiotensin 1, which goes to the lung, gets converted by ACE to AT2, which then vasoconstricts, and also binds to the zona glomerulosa to induce aldosterone synthesis, which then acts on the collecting ducts
 
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But how does angiotensin 2 -->more aldosterone in zona glomerulosa to induce aldosterone synthesis?
What's the mechanism and what does ACTH has to do with aldosterone synthesis (if any) ?
 
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If a complete mole contains 46 chromosomes, why didn't it develop into a fetus? Was there something necessary in the ovum for development?
 
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dfib slim said:
If a complete mole contains 46 chromosomes, why didn't it develop into a fetus? Was there something necessary in the ovum for development?
Click to expand...

the 46 chromosomes comes purely from the father.
FA "Most commonly enucleated egg + single sperm (subsequently duplicates paternal DNA) "
 
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with the window period of hep B virus, hbE antibody is also present, so doesnt that also correlate with low infectivity? meaning that patients are unlikely to go into a chronic hep with high infectivity?
 
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Krasmyc said:
the 46 chromosomes comes purely from the father.
FA "Most commonly enucleated egg + single sperm (subsequently duplicates paternal DNA) "
Click to expand...
I knew that part, I just wasn't thinking of imprinting as being a possible cause for failure of development.
 
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What are the 4 carcinomas that spread hematogenously (usually carcinoma spreads lymphatically but there are 4 exceptions - according to Dr Sattar in pathoma)?
 
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Can someone pls explain the 3 stages of Acute Tubular necrosis (aka intrarenal azotemia)? Having a little trouble understanding it :/
 
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LAK84 said:
What are the 4 carcinomas that spread hematogenously (usually carcinoma spreads lymphatically but there are 4 exceptions - according to Dr Sattar in pathoma)?
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There are more than 4, but the classic 4 are HCC, RCC, chorio, follicular thyroid. Another one would be ovarian embryonal carcinoma, serous adenocarcinoma as well.
 
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seminoma said:
Cool, I don't feel bad for not knowing that! We're in GI right now 🙂

Actually I'm glad you mention it because it's not in FA.
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I want to say extramammary paget disease as well. You haven't started dedicated yet? How many weeks you get?
 
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dfib slim said:
I want to say extramammary paget disease as well. You haven't started dedicated yet? How many weeks you get?
Click to expand...

We have another two weeks of school. 7 weeks of "summer". I'm taking 6 weeks for dedicated.

I don't remember extramammary pagets having an association with e-cadherin, but you might be right.
 
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dfib slim said:
Not sure. Only heard it "talked about" with a few.
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I think @Transposony is getting at a couple of general concepts about mets. First that the cells aren't inhibited by crowding (can't remember the specific name) and second that they lose ability to attach to each other (e.g. cadherins). Both of those things "help" the cell or group of cells break off from the primary tumor and go elsewhere. The fact that about 30% of lobular carcinomas in the breast are bilateral at the time of diagnosis could be related to the strong association with loss of E-cadherin.
 
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Mechanism of omeprazole.

What cell type? Intracellular or extracellular? Reversible or irreversible? Major electrolyte imbalance with long-term use?
 
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dfib slim said:
If a complete mole contains 46 chromosomes, why didn't it develop into a fetus? Was there something necessary in the ovum for development?
Click to expand...
Transposony said:
Could be due to imprinting since the ovum does have mitochondria.
Click to expand...

Yeah, imprinting. The DNA in a complete mole is all of paternal origin. No fetus is viable without the contribution from male and female parents. There are tons of genes that will be silenced in a complete mole.
 
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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 = ?
 
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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
 
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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
 
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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
 
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Someone have a good way/mnemonic or easy way of remembering the congenital adrenal hyperplasias (21 hydroxylase, 11 beta, 17 alpha)?
I ALWAYS miss small details and screw it up...esp the differences in male vs. female androgen effects, etc... Maybe I should just make 3 flashcards? lol
 
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LAK84 said:
Someone have a good way/mnemonic or easy way of remembering the congenital adrenal hyperplasias (21 hydroxylase, 11 beta, 17 alpha)?
I ALWAYS miss small details and screw it up...esp the differences in male vs. female androgen effects, etc... Maybe I should just make 3 flashcards? lol
Click to expand...
Pathoma vid
 
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LAK84 said:
Someone have a good way/mnemonic or easy way of remembering the congenital adrenal hyperplasias (21 hydroxylase, 11 beta, 17 alpha)?
I ALWAYS miss small details and screw it up...esp the differences in male vs. female androgen effects, etc... Maybe I should just make 3 flashcards? lol
Click to expand...

Start by being able to draw the steroid pathway. Whenever I have a CAH question I always go back to the mental image I have of the pathway and it never fails.
 
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