Official Step 1 High Yield Concepts Thread

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Transposony

Do or do not, There is no try
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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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actually to detect RNA splicing defect we use northern blot.
You just finished saying it "RNA splicing" detect. and we all know that for RNA detection we use northern blot. remember the gene for beta globin is fine. the defect is in the abnormal processing for the primary transcript of RNA.
 
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how hypothyroidsm causing non pitting edema (be specific) ?













@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma

As far as I'm aware thyroid derangement can lead to glycosaminoglycan deposition (e.g., heparan/dermatan sulfate). Pitting implies interstitial fluid accumulation (e.g., kidney/liver/heart disease). Non-pitting seen in lymphatic obstruction and thyroid derangement can be secondary to non-fluid changes; with the former, fibrous tissue can be produced alongside extravasation, similar to the latter's deposition of ECM.
 
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230546_l125.jpg




what is this ? which drug\s can cause it ?
 
230546_l125.jpg




what is this ? which drug\s can cause it ?

One thing I've observed through rotations is that any drug can cause anything. But the drug rashes/eruptions typically fall on the spectrum of morbilliform --> erythema multiforme --> SJS --> TEN. TEN is obvious because of its severity/diffuse involvement. Both SJS and TEN have mucosal involvement, which is what I'd look for here. But in actuality the exact extent of the eruption on the spectrum isn't as important as the mere identification of the aetiology as drug-induced. The symmetry in this picture, notably along the dorsolateral aspects of the feet, suggest a vascular pattern, and could even point toward a drug-induced vasculitis. I'd also be thinking things like ITP, TTP, cryoglobulinaemia, HIT (would look at all meds the pt is on).
 
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Causes of acute and reversible urinary incontinence are provided by the DRIP mnemonic:
Delirium
Restricted mobility, retention
Infection (urinary tract), inflammation (urethritis or atrophic vaginitis), impaction (fecal)
Polyuria (diabetes mellitus, diabetes insipidus, congestive heart failure, and venous insufficiency), pharmaceuticals




any further info about urinary incontinence






@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma
 
Causes of acute and reversible urinary incontinence are provided by the DRIP mnemonic:
Delirium
Restricted mobility, retention
Infection (urinary tract), inflammation (urethritis or atrophic vaginitis), impaction (fecal)
Polyuria (diabetes mellitus, diabetes insipidus, congestive heart failure, and venous insufficiency), pharmaceuticals




any further info about urinary incontinence






@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma

An important point is that you can use drugs (anti-muscarinics) to Tx urge incontinence but not for stress incontinence (pelvic floor exercises; Kegel).
 
I just wanted to thank:

@Phloston
@Transposony
@aspiringmd1015
@Keto
@seminoma

For all of their help thus far (and the many others that drop in to give advice).

I was just wondering how long the people I tagged would be able to keep this up- aka will you be able to keep answering up until next summer for the current M2s taking boards this summer?

Thanks again for all of the help!
 
Glycogen storage diseases :-

1. Von Gierke.- glucose 6 phosphatase deficiency. normal glycogen structure. severe hypoglycemia, hepatomegaly, hyperlipidemia hyperuricemia, short stature doll like faces, protruding abdomen -

2. Pompe - lysosomal alpha 1, 4 glucosidase deficiency. cardiomegaly, muscle weakness, death by 2 years. Glycogen like material in Lysosomes visible.

3. Cori - debranching enzyme deficiency. mild hypoglycemia and hepatomegaly.

4. Anderson - branching enzyme deficiency. infantile hypotonia cirrhosis and death by 2 years.

5. McArdle - muscle glycogen phosphorylase deficiency. muscle cramps weakness on exercise and myoglobinuria.

6. Hers - hepatic glycogen phosphorylase deficiency. mild fasting hypoglycemia and hepatomegaly.
 
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ASA + plavix is never correct. It's ASA then plavix or aggrenox (ASA+dipyridamole).
Just had a UW question suggesting giving ASA + Plavix to a patient with intracranial large artery atherosclerosis who stroked out on ASA. This is opposed to a patient without that atherosclerosis who would get ASA, then Plavix or Aggrenox.
 
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Just had a UW question suggesting giving ASA + Plavix to a patient with intracranial large artery atherosclerosis who stroked out on ASA. This is opposed to a patient without that atherosclerosis who would get ASA, then Plavix or Aggrenox.
That's probably why it came to me from some deep recesses of my mind.
Assuming that it was Step 2 CK QBank.
 
Just had a UW question suggesting giving ASA + Plavix to a patient with intracranial large artery atherosclerosis who stroked out on ASA. This is opposed to a patient without that atherosclerosis who would get ASA, then Plavix or Aggrenox.

News to me and I've completed all the medicine questions. Goes to show how much more we pay attention to Step 1 qbank questions.
 
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A 55 year-old female presents with difficult and painful swallowing, a swollen red tongue and inflammation at the corners of her mouth. Endoscopy of her esophagus reveals the presence of webs and a biopsy of a lesion in her esophagus is concerning for squamous cell carcinoma. Her peripheral blood smear is most likely to reveal which of the following?
a. Heinz bodies
b. Hypochromic microcytosis
c. Macrocytosis and hypersegmented neutrophils
d. Schistocytes
e. Spherocytes
 
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A 50 year-old male with chronic renal failure due to diabetic nephropathy comes to the ER after his family notes that he has been vomiting and confused for the past two days. He has also been complaining of muscle cramps and multiple excoriations are evident on his arms and legs. His family admits that he has missed his last several dialysis appointments because he said that "he didn't like the way they felt". On physical exam, his doctor notes that the patient's neck veins bulge when he is breathing in. This is most likely due to:
a. Increased blood viscosity
b. Inflammation of the pericardium
c. Neurological toxicity
d. Pulmonary embolism
e. Volume overload
 
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A six-month old girl is brought to her new pediatrician with a three-day history of fever. A review of her medical history reveals a consistently high WBC count and delayed umbilical cord separation. Her history is also significant for an infection of her umbilical cord stump with Staphylococcus aureus characterized by cellulitis but notably without pus, and her WBC count at the time was markedly elevated (45 X 109/L). Analysis of her WBCs by flow cytometry is shown below. Which of the following pairs of markers was most likely used to determine the nature of this girl's immunodeficiency?

11224615.jpg
 
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A 55 year-old female presents with difficult and painful swallowing, a swollen red tongue and inflammation at the corners of her mouth. Endoscopy of her esophagus reveals the presence of webs and a biopsy of a lesion in her esophagus is concerning for squamous cell carcinoma. Her peripheral blood smear is most likely to reveal which of the following?
a. Heinz bodies
b. Hypochromic microcytosis
c. Macrocytosis and hypersegmented neutrophils
d. Schistocytes
e. Spherocytes


The presence of swollen red tongue is suggestive of glossitis and the esophageal web are part of this plummer vinson syndrome which is seen in iron defiency. iron defiency would then lead to hypochromic microcytosis on the peripheral blood cell smear.
 
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A 50 year-old male with chronic renal failure due to diabetic nephropathy comes to the ER after his family notes that he has been vomiting and confused for the past two days. He has also been complaining of muscle cramps and multiple excoriations are evident on his arms and legs. His family admits that he has missed his last several dialysis appointments because he said that "he didn't like the way they felt". On physical exam, his doctor notes that the patient's neck veins bulge when he is breathing in. This is most likely due to:
a. Increased blood viscosity
b. Inflammation of the pericardium
c. Neurological toxicity
d. Pulmonary embolism
e. Volume overload

the thing with dialysis is you got to ask what does it aim to do right? i mean guy has renal failure so he needs dialyisis to filter the blood and help with maintaining blood volume. So by missing dialysis, im assuming he is going to have fluid retention because he isnt making urine anytime soon due to renal failure

...anyways, the venous neck bulge with the breathing in harps on a cardiovascular physiology principle that on inspiration, you get increased venous return. And this guy, looks like he had massive venous return since this bulge is visible. so all signs kind of point that this guy has a volume overload problem... e
 
A six-month old girl is brought to her new pediatrician with a three-day history of fever. A review of her medical history reveals a consistently high WBC count and delayed umbilical cord separation. Her history is also significant for an infection of her umbilical cord stump with Staphylococcus aureus characterized by cellulitis but notably without pus, and her WBC count at the time was markedly elevated (45 X 109/L). Analysis of her WBCs by flow cytometry is shown below. Which of the following pairs of markers was most likely used to determine the nature of this girl's immunodeficiency?

View attachment 196886

Leukocyte Adhesion Deficiency
So , The Answer is C ?
 
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what is Heteroplasmy ?
It's having two types of DNA in the same cell organelle.
For example, a cell in which mitochondria having normal mitochondrial DNA and mutated mitochondrial DNA.
This will lead to variable expression since both of them will express and as this Heteroplasmy is passed down the progeny will have even more variable expression since during cell division this DNA (both mitochondrial DNA and a mutated mtDNA) will sort randomly.
The concept is similar to mosaicism e.g. in Turner syndrome.
 
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It's having two types of DNA in the same cell organelle.
For example, a cell in which mitochondria having normal mitochondrial DNA and mutated mitochondrial DNA.
This will lead to variable expression since both of them will express and as this Heteroplasmy is passed down the progeny will have even more variable expression since during cell division this DNA (both mitochondrial DNA and a mutated mtDNA) will sort randomly.
The concept is similar to mosaicism e.g. in Turner syndrome.
Variable expression is variable phenotype between individuals with regard to a condition with 100% penetrance. You can't have more or less variable expression. It's black and white and is either associated with a disease or not. Heteroplasmy is essentially mitochondrial DNA mosaicism.
 
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An individual cell can have more than 1 type of mitochondrial DNA.

For Step 1, heteroplasmy is the answer to any question related to varied penetrance/expressivity (I don't remember or care what the difference is anymore) of diseases with mitochondrial inheritance.

For test taking purposes heteroplasmy is to mitochondrial diseases as anticipation is to trinucleotide repeats.
 
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Good questions @Transposony are they from Becker qbank?

And if someone can please answer one minor weird question for me. Kinases are enzymes that utilize ATP to add a phosphate group onto a substrate, right? Then how come Pyruvate Kinase does not follow this rule? Instead, ATP is produced at the step catalyzed by it (PEP ---> Pyruvate).
Thanks
 
And if someone can please answer one minor weird question for me. Kinases are enzymes that utilize ATP to add a phosphate group onto a substrate, right? Then how come Pyruvate Kinase does not follow this rule? Instead, ATP is produced at the step catalyzed by it (PEP ---> Pyruvate).
Thanks
Kinases catalyzes the transfer of a phosphate group from a high energy molecule (usually ATP) to their substrate molecule.
However, in substrate-level phosphorylation catalyzed by Pyruvate Kinase, phosphoenolpyruvate carries the high energy phosphate bond which is used in the reaction.
 
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A 55 year-old female presents with difficult and painful swallowing, a swollen red tongue and inflammation at the corners of her mouth. Endoscopy of her esophagus reveals the presence of webs and a biopsy of a lesion in her esophagus is concerning for squamous cell carcinoma. Her peripheral blood smear is most likely to reveal which of the following?
a. Heinz bodies
b. Hypochromic microcytosis
c. Macrocytosis and hypersegmented neutrophils
d. Schistocytes
e. Spherocytes

A 50 year-old male with chronic renal failure due to diabetic nephropathy comes to the ER after his family notes that he has been vomiting and confused for the past two days. He has also been complaining of muscle cramps and multiple excoriations are evident on his arms and legs. His family admits that he has missed his last several dialysis appointments because he said that "he didn't like the way they felt". On physical exam, his doctor notes that the patient's neck veins bulge when he is breathing in. This is most likely due to:
a. Increased blood viscosity
b. Inflammation of the pericardium
c. Neurological toxicity
d. Pulmonary embolism
e. Volume overload

A six-month old girl is brought to her new pediatrician with a three-day history of fever. A review of her medical history reveals a consistently high WBC count and delayed umbilical cord separation. Her history is also significant for an infection of her umbilical cord stump with Staphylococcus aureus characterized by cellulitis but notably without pus, and her WBC count at the time was markedly elevated (45 X 109/L). Analysis of her WBCs by flow cytometry is shown below. Which of the following pairs of markers was most likely used to determine the nature of this girl's immunodeficiency?

View attachment 196886

Thanks a lot @Transposony for the explanation.
As for my other question, the questions you posted are they from Becker qbank? I'm thinking of trying it out that's why asking. I liked these questions you posted. Thanks
 
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