Official Step 1 High Yield Concepts Thread

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
Transposony

Transposony

Do or do not, There is no try
10+ Year Member
Joined
Nov 10, 2011
Messages
1,810
Reaction score
999
Members don't see this ad.
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
 
Last edited:
Sort by date Sort by votes
with MDS, sattar says that the blasts in the bone marrow are less than 20%, and patients will have cytopenias bc of the dysplastic growth within the bone marrow, but will be leukemia once the blasts take up >20% of the bone marrow, so its after this 20% mark, when the blasts enter the blood to be actually defined as a leukemia?
 
Upvote 0 Downvote
dfib slim said:
And benzocaine. Also, you give amyl nitrite to induce methemoglobinemia to treat cyanide poisoning.
Click to expand...
this is because MetHb has higher affinity for CN and can remove it from the circulation, thus decreasing its toxic effects on Mito; can also give thiosulfate to bind CN to become thiocyanate, which is excreted
 
Upvote 0 Downvote
Transposony said:
Effect of Barbs/Benzo on pain ?

Name the receptor through which Opiates reduces pain.

Aprepitant acts via which receptor?

Nonbenzodiazepines acts via which receptor?
Click to expand...

barbs/benzo don't work for pain??
opiates work on mu receptors
aprepitant is a substance P antagonist, antiemetic, blocks neurokinin 1 receptor
nonbenzos act via BZ1 subreceptor of GABA receptor, reversed by flumazenil
 
Upvote 0 Downvote
dfib slim said:
How would you distinguish between serotonin syndrome and neuroleptic malignant syndrome clinically?
Click to expand...
Serotonin syndrome: Increased serotonin-------->Increased NeuroMuscular excitability like hyperreflexia & myoclonus.
NMS: Decreased Dopamine (similar to Parkinson's)---->Decreased NeuroMuscular excitability like bradyreflaxia & rigidity.

Onset duration is also helpful (acute for SS as compared to subacute for NMS)
 
Upvote 0 Downvote
Edit: NM i figured it out. Ill turn it into a question

Are you more likely to get same gender twins in monozygotic twins or dizygotic twins?
 
Upvote 0 Downvote
NoLollipops4U said:
I wrote down in my FA (I guess from UW?) that monozygotic twins are the same gender, where as dizygotic twins can be same or different gender

Is there any truth to this? I can't reason why this would be true as an absolute. Thanks
Click to expand...
It's true.
Monozygotic twinning happens when a fertilized zygote splits and forms two embryos. They are identical copies of each other so they only be both male or both female.
Dizygotic twinning happens when two different eggs get ovulated and fertilized. They can be different or the same sex.
 
Upvote 0 Downvote
saline induced diuresis prevents nephrotoxicity associated with cisplatin. What is the mechanism for this? generally i'd think that saline induced diuresis would be helpful in patients with conditions which decrease renal bloodflow? as saline would increase the blood volume? or is it washing out the metabolites that are accumulating within the kidney?
 
Upvote 0 Downvote
Transposony said:
Serotonin syndrome: Increased serotonin-------->Increased NeuroMuscular excitability like hyperreflexia & myoclonus.
NMS: Decreased Dopamine (similar to Parkinson's)---->Decreased NeuroMuscular excitability like bradyreflaxia & rigidity.

Onset duration is also helpful (acute for SS as compared to subacute for NMS)
Click to expand...
can you also distinguish based on what drugs were given? Typical antipsychotics for NMS and potentially a SSRI + MAOi for serotonin syndrome ?
 
Upvote 0 Downvote
syoung said:
can you also distinguish based on what drugs were given? Typical antipsychotics for NMS and potentially a SSRI + MAOi for serotonin syndrome ?
Click to expand...
They don't give you that info in a vignette. The patient will be unconscious with a psych history and you might have to choose the med they overdosed on based on clinical findings.
 
Upvote 0 Downvote
dfib slim said:
They don't give you that info in a vignette. The patient will be unconscious with a psych history and you might have to choose the med they overdosed on based on clinical findings.
Click to expand...
fair. that's typical of step 1 =/ important to differentiate just based on sx alone
 
Upvote 0 Downvote
Transposony said:
Serotonin syndrome: Increased serotonin-------->Increased NeuroMuscular excitability like hyperreflexia & myoclonus.
NMS: Decreased Dopamine (similar to Parkinson's)---->Decreased NeuroMuscular excitability like bradyreflaxia & rigidity.

Onset duration is also helpful (acute for SS as compared to subacute for NMS)
Click to expand...

Mydriasis is also seen in SS but not NMS which can be helpful
 
Upvote 0 Downvote
Transposony said:
Mechanism behind Loop and Thiazide diuretic use in hypertension?
Click to expand...
loop blocks na/cl/k reuptake in LOH, thus causing diuresis and decreasing volume -> lowers BP; can cause hypocalcemia
thiazide blocks na/cl reuptake in DCT, doing the same as above -> can cause hypercalcemia

both are K wasters, ie does not spare K, so both will lead to hypoK
 
Upvote 0 Downvote
Last edited:
Upvote 0 Downvote
Transposony said:
Yes that's what explains their long term effect on hypertension.
Similarly, loop diuretics has a vasodilatory effect via prostaglandins.
Not sure how much relevant it is for Step 1 though.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904515/

http://www.cvpharmacology.com/diuretic/diuretics
Click to expand...

Had a question about long-term chronic arthritis patient with hypertension and just started on loop diruetic, but wasn't seeing any improvement in his HTN. Question asked what was the most likely cause and the answer was reduced efficacy of loop diuretic due to concurrent NSAID use.
 
Upvote 0 Downvote
Upvote 0 Downvote
CodeRedDew said:
Had a question about long-term chronic arthritis patient with hypertension and just started on loop diruetic, but wasn't seeing any improvement in his HTN. Question asked what was the most likely cause and the answer was reduced efficacy of loop diuretic due to concurrent NSAID use.
Click to expand...

I wonder if it's because:

PGs normally help kidneys maintain GFR by dilating Aff > Eff; NSAIDs disturb this and lead to constriction of Aff > Eff -> less perfusion and less GFR and kidneys don't like this so they rev up RAAS, which ultimately makes AII. AII constricts Eff > Aff, to increase GFR, decrease RPF and increase FF. This would counteract diuretics (to promote Na and therefore H2O excretion)

yes no?
 
Upvote 0 Downvote
What histological findings would you expect of hepatocytes or the ducts in the following:

-HAV infection
-HBV/HCV infection
-Reyes
- reaction to halothane
-alcoholic cirrhosis

Whats a councilman body? When do you see it?
 
Upvote 0 Downvote
Also, can someone explain to me why we don't give beta-blockers in acute decompensated heart failure? The only way I can reason this out is that if the heart failure it acute -->atria can't compensate with an increase in compliance --> pulmonary edema......and BB in pulmonary edema would make it even harder to get oxygen. Is this the correct way to reason it out? Thanks
 
Upvote 0 Downvote
seminoma said:
Acrolein accumulation. Don't know any more than that and I don't think we have to.
Click to expand...
except that MESNA is a sulfhydryl donor which binds with the vinyl group and detoxifies acrolein leading to increased urinary excretion of cysteine.
It's MOA is similar to acetylcysteine.
 
Upvote 0 Downvote
NoLollipops4U said:
Also, can someone explain to me why we don't give beta-blockers in acute decompensated heart failure? The only way I can reason this out is that if the heart failure it acute -->atria can't compensate with an increase in compliance --> pulmonary edema......and BB in pulmonary edema would make it even harder to get oxygen. Is this the correct way to reason it out? Thanks
Click to expand...
Probably because beta-blockers can cause AV block which would be bad in decompensated HF
 
Upvote 0 Downvote
Quick and dirty method of differentiating stenotic from regurgitant valvular lesions on Pressure-volume loop diagram ?
 
Upvote 0 Downvote
pH low think a) low bicarb- metabolic acidosis or b) high CO2- resp acidosis
pH high think a) high bicarb- metabolic alkalosis or b) low CO2- resp alkalosis
now check for compensation: if primary is metabolic, respiratory compensation is fast and in same direction as the metabolic change (check me?), but never enough to get pH back to normal; if primary is respiratory, metabolic compensation is slow and takes an extra day or so since the kidneys has to either hold onto more bicarb or get rid of more, but it's also in the same direction as the respiratory change, but never enough to get pH back to normal
 
Upvote 0 Downvote
Acid Base Mnemonic: ROME

R: Respiratory (Acidosis and Alkalosis)
O: Opposite: pH ↓ and CO2 ↑ = Acidosis; pH ↑ CO2 ↓ = Alkalosis
M: Metabolic (Acidosis and Alkalosis)
E: Equal: pH ↓ and HCO3 ↓ = Acidosis; pH ↑ & HCO3 ↑ = Alkalosis

Remember, compensation NEVER fully restores the pH to normal. It is ALWAYS just short of normal pH.
 
Upvote 0 Downvote
what should you be wary of/supplement when using a drug that decreases synthesis of mycolic acid as prophylaxis?
 
Upvote 0 Downvote
You must log in or register to reply here.

Similar threads

Transposony
Official 2024 Step 1 Experiences and Scores Thread
Replies
0
Views
2K
Transposony
Transposony
C
Step 1 tutor available!
Replies
0
Views
937
chauhanjugalkishor
C
A
USMLE Step 1 resources for sale
Replies
0
Views
2K
accurate_branch20
A
D
Step 1 and Level 1
Replies
1
Views
2K
DOcSto
D
C
USMLE Understanding Public Health in STEP 1?
Replies
0
Views
1K
Cheerios5789
C
Top