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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What is the mechanism by which epo synthesis is down regulated in the presence of adequate oxygen,(specific mechanism involving HiF)?
 
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Which antifungal can cause QT prolongation?

Which Antibiotic can cause black tongue?

What Pathology is associated with missense or point mutation of FGFR3? (hint :not overexpression of it)
 
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Name the hepatitis virus- associated disease/s (and the corresponding virus HBV/HBC) in:
- Skin
- Kidney
- Blood
- Vasculature
 
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Radiolucent said:
Name the hepatitis virus- associated disease/s (and the corresponding virus HBV/HBC) in:
- Skin
- Kidney
- Blood
- Vasculature
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HBV Membranous glonerulobeprhritis in kidney, MPGN type 1(less so than C) serum sickness like reaction in blood. PAN in kidney, skin, blood.

HCV lichen planus in skin, cryoglobulinemia in blood, type 1 MPGN, Membranous glomerulonephritis (less than B) in kidney, porphyria in blood.

That's all I can think of I thibk there night be 1 of 2 more.
 
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I wouldn't say these are high yield, but along the lines of what others posted in the thread before. "sdn high yield"
 
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Kingella said:
HBV Membranous glonerulobeprhritis in kidney, MPGN type 1(less so than C) serum sickness like reaction in blood. PAN in kidney, skin, blood.

HCV lichen planus in skin, cryoglobulinemia in blood, type 1 MPGN, Membranous glomerulonephritis (less than B) in kidney, porphyria in blood.

That's all I can think of I thibk there night be 1 of 2 more.
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Very nice, now I feel like I have to study some more..
 
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Radiolucent said:
All cause RPGN (nephritic syndrome):
- Goodpasture syndrome: Hematuria, hematoptysis. Anti-GM ab --> linear depostion on IF.
- Granulomatosis with polyangitis (Wegeners): Granulomas in upper+lower resp tract (can cause hematoptysis) + kidneys (hematuria). c/PR3-ANCA + , - IF (pauci-immune)
- Microscopic polyangitis: Necrotizing vasculitis (w/o granulomas) in lower resp tract only (vs Wegeners) + kidney involvement. p/MPO-ANCA +, - IF

Once again: Primary biliary cirrhosis vs Primary sclerosing cholangitis (in terms of histopath/autoantibodies)?
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sclerosing cholangitis has p-anca, onion (skin or peel?) appearance, beading of ducts,
biliary cirrhosis- anti mitochondrial antibodies. i think maybe copper deposition and granulomas ?
 
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Kingella said:
sclerosing cholangitis has p-anca, onion (skin or peel?) appearance, beading of ducts,
biliary cirrhosis- anti mitochondrial antibodies. i think maybe copper deposition and granulomas ?
Click to expand...
remembering the p-anca for slerosing cholangitis helps me remember the UC association.
 
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Kingella said:
sclerosing cholangitis has p-anca, onion (skin or peel?) appearance, beading of ducts,
biliary cirrhosis- anti mitochondrial antibodies. i think maybe copper deposition and granulomas ?
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Kingella said:
remembering the p-anca for slerosing cholangitis helps me remember the UC association.
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Spot on. Also, remember the ASCA association to Chron´s.
 
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Kingella said:
yep. also NOD-2 mutation which I saw for the first time in uworld.
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led me to google NOD, which produced this
latest

which looks like a colon to me, but i have no idea what it actually is, looks like some sort of game.
 
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Idk I just took a guess and since it's an open ended question the first thing that came to mind was what I studied yesterday which is biochem haha.
Yea vitamin or nutritional deficiency sounds more likely although I think any question would have clues that point to that.
 
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Why does iron deficiency/megaloblastic anemia lead to a falsely elevated hemoglobin A1C? Something about increased RBC lifespan but not sure of the cause...
 
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dfib slim said:
Why does iron deficiency/megaloblastic anemia lead to a falsely elevated hemoglobin A1C? Something about increased RBC lifespan but not sure of the cause...
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This is very low yield but here goes: decreased oxygen carrying capacity of the blood -> decreased ATP generation of cells peripherally -> decreased ability to metabolize ROS species (via decreased NADPH production, using every glucose for ATP instead) -> increase membrane and fatty peroxidation -> one of the break down products is malondialdehyde, which is a peroxidized fat molecule that broke down -> can be non-enzymatically added (aldehydes are relatively 'hot' electrophiles, any hydroxyl group is likely nucleophilic enough to attack it) to proteins including hemoglobin -> "false positive" HbA1C (HbA1C can't differentiate between what is added to hemoglobin, just that there are extra carbon molecules added, but I also think that there's some way that malondialdehyde increases glycation of Hb)
 
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Kingella said:
I wouldn't say these are high yield, but along the lines of what others posted in the thread before. "sdn high yield"
Click to expand...

Yeah lol. Big difference between "high yield" and "obscure fact" or "difficult concept".

With that said.. sorry if this isn't high yield, but I think it is considering the half-page the layers get in FA. UW says pyloric stenosis is due to hypertrophy of the muscularis mucosae. This didn't make sense to me so I looked at Robbins, which says muscularis propria.. which makes more sense considering that's the actual layer that constricts/relaxes.
 
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seminoma said:
Yeah lol. Big difference between "high yield" and "obscure fact" or "difficult concept".

With that said.. sorry if this isn't high yield, but I think it is considering the half-page the layers get in FA. UW says pyloric stenosis is due to hypertrophy of the muscularis mucosae. This didn't make sense to me so I looked at Robbins, which says muscularis propria.. which makes more sense considering that's the actual layer that constricts/relaxes.
Click to expand...
Can't believe UW would make such a rookie mistake. More specifically it's the circular layer of the muscularis propria.

335px-GI_Organization.svg.png
 
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why does neonatal RDS lead to metabolic acidosis?
and also FA mentions that the fio2 is decreased, how is that possible? the franction of o2 in room air would remain 21 percent wouldnt it?
 
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aspiringmd1015 said:
why does neonatal RDS lead to metabolic acidosis?
and also FA mentions that the fio2 is decreased, how is that possible? the franction of o2 in room air would remain 21 percent wouldnt it?
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Poor tissue perfusion --> metabolic acidosis
FA says low O2 tension, which is PaO2, not FiO2. If you're referring to "low PaO2/FiO2" in the ARDS section, that's talking about the ratio. You expect PaO2/FiO2 to be around 500 (i.e. 105/0.21) in a normal person. The severity and mortality of ARDS correlates with the PaO2/FiO2 ratio (i.e. PaO2/FiO2 of 100 has a much worse prognosis than PaO2/FiO2 of 300)
 
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in Chronic bronchitis, you have mucus plugs which prevent C02 from being exhaled physically, makes sense, but in emphysema, if youre having a problem in exhaling as well(more of a physiological obstruction, shouldnt C02 also be retained? in emphyema your surface area laso thicken so your A- gradient is increased as well, so..?
 
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aspiringmd1015 said:
in Chronic bronchitis, you have mucus plugs which prevent C02 from being exhaled physically, makes sense, but in emphysema, if youre having a problem in exhaling as well(more of a physiological obstruction, shouldnt C02 also be retained? in emphyema your surface area laso thicken so your A- gradient is increased as well, so..?
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Emphysema patients compensate. Hence pink puffers. Cb can't compensate.
 
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compensate by hyperventilation? btw another question lol, giving saline induced diureses helps ampho B toxicity, and other nephrotoxic drugs how? whats the mechanism? maintaining GFR?
 
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Can you aspirate something, yet not get pneumonia? ie in goljan auido, he states that the most common cause of a lung abcess is aspiration, but pneumonia caused by staph and klebs can also do it
 
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faisal 2000 said:
which autoimmune disease causes GERD ? and how ??
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sjogren syndrome is autoimmune disease characterized by lymphocytic infiltration of lacrimal and salivary gland causing dry mouth and eyes.normally saliva is rich in bicarbonate which neutralize acid in esophagus, so in sjogren syndrome absence of saliva will leads to esophagus damage with even GERD .
 
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What are the different types of hypertension that a patient can have? (give risk factor, any relevant pathology)
What is the mechanism of opioids? What 5 substances do they prevent from being released?
 
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theTruth_97 said:
What are the different types of hypertension that a patient can have? (give risk factor, any relevant pathology)
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Primary (idiopathic) HTN:
Polygenic, various mechanisms (IIRC Liddle syndrome counts as primary?).
Risk factors: age, sex (male), type A personality disorder, smoking, race (blacks), DM, obesity.

Secondary HTN:
MCC: Renovascular causes: Fibromuscular dysplasia, renal artery stenosis, AD/AR-PKD. --> causes activation of RAAS-system
Obstructive sleep apnea
Endocrine causes: Conns syndrome (hyperaldo), Pheochromocytoma (also neuroblastoma), Cushings syndrome/disease, hypercalcemia, hyperthyroidism, renin secreting neoplasms, acromegaly
Liqurice consumption.
Pregnancy related: HELLP syndrome, pre/ecclampsia.
Drugs.

I´m pretty sure there are a lot more but those are the ones I could come up with now.

theTruth_97 said:
What is the mechanism of opioids? What 5 substances do they prevent from being released?
Click to expand...

Opens K+ channels, close Ca2+ channels. Inhibits release of acetylcholine, norepi, sbstance P, glutamate and serotonin.
 
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