Official Step 1 High Yield Concepts Thread

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

Transposony

Do or do not, There is no try
10+ Year Member
Joined
Nov 10, 2011
Messages
1,811
Reaction score
999
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

Members don't see this ad.
 
Last edited:
  • Like
Reactions: 5 users
That's a moot point since Gatifloxacin has been removed from the market as it causes dysglycemia.
So, they are unlikely to ask about it one the test.

Idk I've heard about muromonab and pergolide showing up. Both of those have been off the market.
 
Members don't see this ad :)
Idk I've heard about muromonab and pergolide showing up. Both of those have been off the market.
I agree with you since it is USMLE.
But, there is a difference.
Muromonab was voluntarily withdrawn from the United States market due to decreased utilization but still used in rest of the world.
Pergolide was withdrawn from the U.S. market but still used in rest of the world.
In contrast, Gatifloxacin has been removed from the market and it is no longer being manufactured.
 
  • Like
Reactions: 1 user
Great.
To summarize the differentiating feature are:
Atropine poisoning --> dry skin (Muscarinic block as sweating is sympathetic muscarinic mediated)
TCA overdose --> dry skin with arrhythmia and hypotension (Muscarinic and alpha 1 block)
Amphetamine toxicity --> warm and sweaty skin (as sweating is sympathetic muscarinic mediated)
They all have s/s of sympathetic over-activity.
- atropine poisoning treated by physostigmine
- tca overdose treated by sodium bicarbonate (NaHCO3)
-amphetamine toxicity treated by ??????
-opioid poisoning treated by naltrexone (long acting)
 
  • Like
Reactions: 1 user
Great.
Atropine poisoning --> dry skin (Muscarinic block as sweating is sympathetic muscarinic mediated)
TCA overdose --> dry skin with arrhythmia and hypotension (Muscarinic and alpha 1 block)
Amphetamine toxicity --> warm and sweaty skin (as sweating is sympathetic muscarinic mediated)
They all have s/s of sympathetic over-activity.
benzodiazepine overdoses result in mydriasis, tachycardia, disruption of sleep pattern
treated by Flumazenil
 
Don't know the answer to this, so hopefully one of you can provide a fairly comprehensive explanation.

Why does thiamine deficiency cause vasodilation? I know that thiamine deficiency reduces ATP synthesis, but why does this dilate arterioles?


I agree with you since it is USMLE.
But, there is a difference.
Muromonab was voluntarily withdrawn from the United States market due to decreased utilization but still used in rest of the world.
Pergolide was withdrawn from the U.S. market but still used in rest of the world.
In contrast, Gatifloxacin has been removed from the market and it is no longer being manufactured.

Wow, did not know!
 
Don't know the answer to this, so hopefully one of you can provide a fairly comprehensive explanation.

Why does thiamine deficiency cause vasodilation? I know that thiamine deficiency reduces ATP synthesis, but why does this dilate arterioles?
Nobody knows for sure so they can't ask it on the test.
However, it's been postulated that since AMP can't be converted to ATP, it gets converted to adenosine which accumulates intracellulary and gets pumped out into plasma causing vasodilation.
 
  • Like
Reactions: 1 user
Members don't see this ad :)
Name two bacteria whose capsule makes them non-immunogenic and why?

Strep pneumo
H influenzae
Neisseria
GBS
klebsiella
salmonella typhi
psuedomonas aeruginosa
cryptococcus neoformans (fungi)

SHiN Kills Some Patients with Capsules
Strep, H influenza, klebsiella, salmonella, pseudomonas, cryptococcus

others:
e. coli, bordatella, strep pyogenes, anthrax
 
Strep pneumo
H influenzae
Neisseria
GBS
klebsiella
salmonella typhi
psuedomonas aeruginosa
cryptococcus neoformans (fungi)

SHiN Kills Some Patients with Capsules
Strep, H influenza, klebsiella, salmonella, pseudomonas, cryptococcus

others:
e. coli, bordatella, strep pyogenes, anthrax
I think you misread the question.
 
Aren't they immunogenic, esp if you have no spleen, are young w/out a developed immune system? Because of their polysaccharide capsule?

I think he's talking about GAS (hyaluronic acid capsule) and B-type N.meningititis.. or however you spell that.
 
Err I meant to say "Aren't they non-immunogenic"...
I think we are going in circles here.
As Seminoma said, Streptococcus pyogenes due to hyaluronic acid and type b Neisseria meningitidis due to sialic acid.
These make their capsule non-immunogenic and it is the reason why there is no vaccine against type b Neisseria meningitidis.
 
  • Like
Reactions: 1 user
  • Like
Reactions: 1 user
  • Like
Reactions: 1 user
sodium%20channel%20subclass%20effects.gif


Sodium-channel blockade:
IC > IA > IB

Increasing the ERP:
IA > IC > IB (decreases)

http://www.cvpharmacology.com/antiarrhy/sodium-blockers.htm

http://www.pharmacology2000.com/Cardio/antiarr/antiarrtable.htm
 
  • Like
Reactions: 1 users
Mechanism of flatulence in Giardiasis?


Dimorphic Fungii Mnemonic:
Body Heat Changes Shape
Blasto, Histo, Coccidio, Sporothrix
 
Last edited:
Mechanism of action of Chloroquine and it's limitations ?

Blood disorders which prevent against Malaria?
 
Hm, interesting find about L. monocytogenes. That has always been one of the many random factoids I've committed to memory for micro (FA/Microcards). FA 2015 has it in there.
 
Difference between Carcinoid disease and syndrome ?

Vitamin deficiency associated with pheochromocytoma?
 
Difference between Carcinoid disease and syndrome ?

Vitamin deficiency associated with pheochromocytoma?
Isn't it carcinoid disease when you have a GI tumor causing increased release of serotonin with diarrhea and syndrome when that tumor metastasizes to the liver and you get right heart valvular fibrosis?

Haven't learned about pheo yet. Maybe vitamin D since cholesterol is the precursor?
 
Isn't it carcinoid disease when you have a GI tumor causing increased release of serotonin with diarrhea and syndrome when that tumor metastasizes to the liver and you get right heart valvular fibrosis?

Haven't learned about pheo yet. Maybe vitamin D since cholesterol is the precursor?
I meant Carcinoid tumor v/s Carcinoid syndrome.
GI tract carcinoid tumors release serotonin into the hepatic portal circulation which usually undergoes hepatic degradation and therefore does not produce symptoms. However, carcinoid tumors like ovarian which drain into systemic circulation will still cause symptoms.
Carcinoid syndrome occurs when the tumor is so advanced that it overwhelms the liver's ability to metabolize the released serotonin, usually due to metastasis.
It is aka malignant carcinoid.

Vitamin C deficiency is associated with pheochromocytoma since Vit C is a necessary co-factor for dopamine β-hydroxylase, which converts dopamine to NE.


It is similar to Niacin deficiency occuring in carcinoid syndrome as a result of increased tryptophan metabolism into serotonin (tryptophan is diverted to form 5-hydroxytryptophan).


220px-Pellagra2.jpg
 
Last edited:
  • Like
Reactions: 1 users
  • Like
Reactions: 1 user
Top