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
1,810
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
 
Last edited:
Patient with no other important history other than recurrent otitis media has been recently hospitalized due to injuries sustained in a motor vehicle accident. The patient had massive hemorrhaging and blood transfusions were given. Shortly after administration of the blood product, the patient begins to develop a rash and wheezing. What is the pathophysiology causing the patients symptoms?
Selective IgA Deficiency (reactions after receiving blood tranfusion due to IgG anti-IgA antibodies). Less commonly can also form IgE antibodies.
Associated with celiac disease.
 
Last edited:
Selective IgA Deficiency (reactions after receiving blood tranfusion due to IgG anti-IgA antibodies). Less commonly can also form IgE antibodies.
Associated with celiac disease.
you're much more specific..

also i shoulda have known the selective IgA def b/c i got a ? wrong on it in Uworld -_-
 
variable expressivity is when a mutation does not confer the same phenotypes in the people who have it. IE there's a diseases that's AD (everyone in every generation gets it) but each person has a different spectrum of disease
allelic heterogeneity is when multiple mutations at a single locus cause the same phenotype. IE there's a disease where all it takes is one difference in bp from consensus sequence or there's additional copies of the gene compared to the general population and BOOM you have the disease
 
variable expressivity is when a mutation does not confer the same phenotypes in the people who have it. IE there's a diseases that's AD (everyone in every generation gets it) but each person has a different spectrum of disease
allelic heterogeneity is when multiple mutations at a single locus cause the same phenotype. IE there's a disease where all it takes is one difference in bp from consensus sequence or there's additional copies of the gene compared to the general population and BOOM you have the disease


Thank you!
 
Estrogens effect is prothrombotic, but why does it have no effect on factor 9, and does estrogen simply just send signals to the liver to increase synthesis of these factors like it does with sex hormone binding globulin? or does it effect it by increasing the activated amount of the vit k dependent coag factors by interacting with vitamin k somehow?
 
If a pt has endometrial Ca, what drug/what can you do to treat the menopause symptoms?

Well, I think in general you would probably just want to avoid using any type of MHT (menopausal hormone therapy) with endometrial cancer. What you could use is a SSRI/SNRI instead
 
Well, I think in general you would probably just want to avoid using any type of MHT (menopausal hormone therapy) with endometrial cancer. What you could use is a SSRI/SNRI instead
Could you also use cyclic progesterone? That way it can tone down the hyperplasia of the endometrium and help slough it?
 
perhaps surgery to remove the uterus, TAHBSO, then give MHT

the cyclical progesterone is probably only effective if it were endometrial hyperplasia in a post-menopausal woman and not endometiral Ca
 
thats another fair point, patients with endometrial hyperplasia usually have estrogen excess, so would they even have menopausal symptoms?
 
perhaps surgery to remove the uterus, TAHBSO, then give MHT

the cyclical progesterone is probably only effective if it were endometrial hyperplasia in a post-menopausal woman and not endometiral Ca

Problem is a patient with endometrial CA is also at greater risk for breast CA and so I would still be wary of using an MHT

According to uptodate, you should avoid using an MHT and try a SSRI or SNRI instead (cannot find the section today but last night I swear that's what I read)
 
Last edited:
nice. Pt with IgM mediated Immune hemolytic anemia, whats the mechanism behind association with mycoplasma pneumoniae and infectious mono?
 
IgM mediated immune hyemolytic anemia, esp if cold IgM, can be brought on by high titers of IgM antibodies in mycoplasma pneumoniae and infectious mono
 
1. Timely administration of antibiotics to a patient with S. pyogenes will prevent what autoimmune-related complication?

2. What will antibiotics not prevent?
 
with sickle cell trait, it says the rbcs have less than 50% hbS. Does that mean within the rbc each rbc has <50%? or 50% of the entire volume of rbc have HbS only within them, and 50% have hbA
 
with sickle cell trait, it says the rbcs have less than 50% hbS. Does that mean within the rbc each rbc has <50%? or 50% of the entire volume of rbc have HbS only within them, and 50% have hbA

It means overall there is <50% HbS. In general that means most RBCs will have <50%, but obviously some might have more than 50%.. Just like if the general population is 60% men and 40% women, most schools will have less women than men, but some might have more.
 
in the first aid errata for 2015, it says in lead poisoning that protoporphyrin should be down instead of up, but in first aid it says it should be up. Shouldnt it be up bc its inhibitting ferrochelatase? even though its inhibitting ala dehydratase too, i thought this inhibition wasnt a complete inhibiton? can anyone clarify this?
 
A frantic NP requires assistance in the emergency room after administering 10x the correct dose of a beta2-agonist to an asthmatic. To make this a learning opportunity for the NP you ask what are common symptoms of beta2-agonist overdose. Which of the following symptoms that the NP lists for you is NOT a side effect of beta2-agonist overdose?

Tachycardia
Palpitations
Bronchodilation
Tremor
Nervousness
Headache
 
A frantic NP requires assistance in the emergency room after administering 10x the correct dose of a beta2-agonist to an asthmatic. To make this a learning opportunity for the NP you ask what are common symptoms of beta2-agonist overdose. Which of the following symptoms that the NP lists for you is NOT a side effect of beta2-agonist overdose?

Tachycardia
Palpitations
Bronchodilation
Tremor
Nervousness
Headache

beta2 agonists overdoses can lead to beta1 agonism, so there'd be tachycardia, palpitations, bronchodilation, tremor and nervousness... so no headache? or is there headache b/c of the vasodilatory properties of beta2 agonism on vasculature.... then my second guess is tremor
 
I'd say bronchodilation. Maybe the bronchi are already maxed out on dilation before you hit overdose concentration.

i'd go with that answer as well. bronchodilation due to de-sensitization of the beta-receptor

Good calls guys.

Bronchodilation is actually the opposite of what would occur. In beta2-agonist overdose, the beta2 receptors become desensitized and thus the patient will actually have bronchoconstriction as a result
 
Good calls guys.

Bronchodilation is actually the opposite of what would occur. In beta2-agonist overdose, the beta2 receptors become desensitized and thus the patient will actually have bronchoconstriction as a result
What condition would you observe the "scotty dog" sign?
 
Good calls guys.

Bronchodilation is actually the opposite of what would occur. In beta2-agonist overdose, the beta2 receptors become desensitized and thus the patient will actually have bronchoconstriction as a result

I don't follow... If you get bronchoconstriction due to desensitization, then why would tremor still occur? Wouldn't all beta-2s be desensitized, thus tremor wouldn't occur?

What condition would you observe the "scotty dog" sign?

Isn't scotty dog a normal finding in the lumbar spine? I guess any pathology of lumbar vetebra would be the answer here?
 
Vitamin deficiency leading to ataxia and impaired position and vibration sense with an MCV of 90 fL?
 
Effect of Barbs/Benzo on pain ?

Name the receptor through which Opiates reduces pain.

Aprepitant acts via which receptor?

Nonbenzodiazepines acts via which receptor?
 
Last edited:
Top