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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Former substance abuser presents with tremor, bradykinesia, rigidity, and postural instability.
Cause and mechanism?
 
The combination of symptoms sounds like a parkinsonian-like drug side effect to me, which could be from a D2-R antagonist, such as an antipsychotic.

Former substance abuser presents with tremor, bradykinesia, rigidity, and postural instability.
Cause and mechanism?
 
Female with persistent pains on her entire body, suspected as fibromayalgia, is seen in the clinic. She came into the clinic today because of persistent rhinitis. You observe nasal polyps in her nose. She also tells you that she has symptoms suggestive of asthma. What is the cause? Underlying mechanism?
 
Female with persistent pains on her entire body, suspected as fibromayalgia, is seen in the clinic. She came into the clinic today because of persistent rhinitis. You observe nasal polyps in her nose. She also tells you that she has symptoms suggestive of asthma. What is the cause? Underlying mechanism?
aspirin intolerant causes nasal polyp and asthma.persistent pains on her entire body may due to that Salicylic acid is irritating to her skin and mucosa and destroys epithelial cells
 
aspirin intolerant causes nasal polyp and asthma.persistent pains on her entire body may due to that Salicylic acid is irritating to her skin and mucosa and destroys epithelial cells

Yes, but the mechanism: aspirin blocks COX -> increased leukotriene actions, which is what causes the asthma
 
The combination of symptoms sounds like a parkinsonian-like drug side effect to me, which could be from a D2-R antagonist, such as an antipsychotic.
The keyword here is substance abuse.
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a neurotoxin precursor to MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. MPTP may be accidentally produced during the manufacture of MPPP, a synthetic opioid drug with effects similar to those of morphine and meperidine.
 
The keyword here is substance abuse.
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a neurotoxin precursor to MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. MPTP may be accidentally produced during the manufacture of MPPP, a synthetic opioid drug with effects similar to those of morphine and meperidine.

Haha well I've never even heard of this I don't think... this is high yield? Is this in first aid ?
 
Haha well I've never even heard of this I don't think... this is high yield? Is this in first aid ?

I don't think it's in FA. Probably not very HY compared to the other things they could ask about Parkinson's disease. They are probably more likely to ask something about the neurophys, pathophys, or pharmacology of PD. There are some pretty interesting neuroimaging findings becoming more common in diagnostics, like the DATSCAN, but I don't think they would ask something like this. There's also a newer imaging finding called the "swallowtail sign." Again, not super HY. PD is still a clinical diagnosis, but these imaging modalities are becoming more commonplace. I would guess that at some point these images may be incorporated into board exams, but I'm not entirely sure that they would fit within the scope of Step 1.
 
Can someone please explain why lab studies in hepatitis reveal just prolonged PT rather than prolonged PT and PTT. Thanks.
 
Can someone please explain why lab studies in hepatitis reveal just prolonged PT rather than prolonged PT and PTT. Thanks.

I would assume they actually prolong both. However PT is the better choice to monitor liver function since it assesses F7 which has the shortest half life of the coag. factors. Shortest half life would mean that the test that evaluates it would be abnormal first. Idk if this is exactly right, just my assumption lol
 
Which two amino acids are recommended to supplement in a patient with pyruvate dehydrogenase deficiency?
 
Which lung disease predisposes patients to TB infection? Which cell does it affect that leads to this predisposition?
 
I would assume they actually prolong both. However PT is the better choice to monitor liver function since it assesses F7 which has the shortest half life of the coag. factors. Shortest half life would mean that the test that evaluates it would be abnormal first. Idk if this is exactly right, just my assumption lol

Thanks. I should have added in my original post that this question arose during a discussion on chronic hepatitis and therefore all factors produced by the liver, including factor IX, would be decreased. Both factors also require vitamin K. So I'm still wondering if there is a scientific basis to testing PT rather than PTT or if it's just protocol.
 
Which lung disease predisposes patients to TB infection? Which cell does it affect that leads to this predisposition?

Silicosis diminishes phagolysosome function of macrophages.

How does smoking affect the risk for mesothelioma in asbestos workers?
 
Thanks. I should have added in my original post that this question arose during a discussion on chronic hepatitis and therefore all factors produced by the liver, including factor IX, would be decreased. Both factors also require vitamin K. So I'm still wondering if there is a scientific basis to testing PT rather than PTT or if it's just protocol.

ahh gotcha. No I don't know if there's a scientific basis or not, sorry! Hopefully someone else can provide some enlightenment
 
Theophylline works by inhibiting PDE and what other mechanism? This second mechanism results in what CNS and what cardiac effects of theophylline?
 
Thanks. I should have added in my original post that this question arose during a discussion on chronic hepatitis and therefore all factors produced by the liver, including factor IX, would be decreased. Both factors also require vitamin K. So I'm still wondering if there is a scientific basis to testing PT rather than PTT or if it's just protocol.
Both will be prolonged in Chronic liver disease and in practice both are done.
However, PT is commonly done since PT reagents are more sensitive to deficiencies of factor VII.
 
Hyaline material in the alveoli along with columnar cells. Located peripherally. Imaging shows consolidation. Non-smoker

Diagnosis?
 
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