Official Step 1 High Yield Concepts Thread

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Transposony

Transposony

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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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doc10487 said:
one of the WTF questions i have heard in a long time

a person goes for the hiking, used bottled water and cooked food. 3 days later present with myalgia, aches, abdominal pain. Dx is worm infection. what is the source of infection?
bites
ticks
fresh water infection

so can we quickly review parasites transmission?

hiking makes me think of tick bite--> which would be either lyme or Ricketsiaa infx. i don't recall worms.
Click to expand...

i'd go w/ fresh water as well, worms don't come from bites or ticks; many of them are fecal-oral or just skin contact for transmission so it's highly likely that's how that person got it
 
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syoung said:
i'd go w/ fresh water as well, worms don't come from bites or ticks; many of them are fecal-oral or just skin contact for transmission so it's highly likely that's how that person got it
Click to expand...
Possible but unlikely since it's bottled water - depends where the water was bottled--mostly it's tap water but some is bottled from "natural springs" so it's possible.
Difficult to answer since it's not a complete question (what are the other choices?).
 
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TheBunkMD said:
Klebsiella granulomatis infection. Oval inclusions found within macrophages (I think).
Presentation? Tx?
Click to expand...

I don't know the specific description of the lesions, but I would say painful genital ulcers with potential inguinal adenopathy. Treatment is doxy?
 
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syoung said:
what is the MoA of probenecid and what can you give it with to prolong that drug's half life? and what's probenecid's toxicities?
Click to expand...
Probenecid being an acid competes with uric acid reabsorption in the kidney thereby increasing their excretion.
Probenecid and penicillins/cephalosporins can be given together as it decreases penicillin's secretion in the PCT.
Since it increases uric acid excretion---> Uric acid stones.
Also, it's a sulfa drug ---so all that jazz about SJ, hemolytic anemia etc.
 
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What are the calcium, phosphate, ALP and PTH levels in the following situations:

1) 72-year-old woman with kyphosis and Hx of left hip fracture from prior fall; no Hx of renal pathology or abnormal urinalyses.

2) 60-year-old man with recent R-sided hearing loss; no tinnitus; no vertigo; favorite baseball cap that he's had for years is a bit more snug.

3) 65-year-old woman with 30-year Hx of T2DM; recent pain in left forearm.

4) 44-year-old man; chronic alcoholic; blood pressure taken in ED causes forearm twitching.

5) 15-year-old boy with childhood Hx of recurrrent pneumonia and bronchiolitis; weight and height both 10%tile; patient does not report anything wrong with stools; no recent travel; petechiae on shoulders.
 
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Transposony said:
What different from allopurinol ?
Imagine getting a question on febuxostat MoA and XO is not among the choices?
Click to expand...

Febuxostat isn't a a purine analogue and its metabolites don't inhibit XO like allopurinols do. IIRC allopurinol = short half life, but its degredation product (catalyzed by XO) has a super long half life == the main effect.
 
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Phloston said:
What are the calcium, phosphate, ALP and PTH levels in the following situations:

1) 72-year-old woman with kyphosis and Hx of left hip fracture from prior fall; no Hx of renal pathology or abnormal urinalyses.

2) 60-year-old man with recent R-sided hearing loss; no tinnitus; no vertigo; favorite baseball cap that he's had for years is a bit more snug.

3) 65-year-old woman with 30-year Hx of T2DM; recent pain in left forearm.

4) 44-year-old man; chronic alcoholic; blood pressure taken in ED causes forearm twitching.

5) 15-year-old boy with childhood Hx of recurrrent pneumonia and bronchiolitis; weight and height both 10%tile; patient does not report anything wrong with stools; no recent travel; petechiae on shoulders.
Click to expand...

@Phloston

1. Normal. Ca, PO4, ALP, PTH are normal in osteoporosis. Unless she's being treated.. but then I think the labs would depend on the regimen.

2. Looks like Paget's. So high ALP, everything else normal.

3. No idea. I would say osteoporosis, but they're asymptomatic until a bone breaks. Osteoarthritis won't start in the forearm. Neuropathy won't change the labs. Charcot joint won't be in the forearm. Honestly the first thing I thought of in this patient was an MI. Older women have atypical presentations plus the longstanding DM as a CV risk factor..

4. Low Ca, high PTH, low PO4, high ALP

5. Don't know. Not CF, maybe Wiskott aldrich, but that wouldn't change these labs, maybe kartageners but again no lab changes...
 
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Pap smear on a 35 year old woman shows CIN III. Terrified, she storms out of your office and you are unable to contact her to discuss prognosis/treatment. She returns 2 years later. At this time you perform another pap smear. What are you most likely to find?

A. Regression of the lesion
B. CIN III
C. CIS
D. Invasive carcinoma without spread to adjacent tissues or mets
E. Mets to obturator and hypogastric nodes
F. Hematogenous lung mets
 
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seminoma said:
@Phloston

1. Normal. Ca, PO4, ALP, PTH are normal in osteoporosis. Unless she's being treated.. but then I think the labs would depend on the regimen.

2. Looks like Paget's. So high ALP, everything else normal.

3. No idea. I would say osteoporosis, but they're asymptomatic until a bone breaks. Osteoarthritis won't start in the forearm. Neuropathy won't change the labs. Charcot joint won't be in the forearm. Honestly the first thing I thought of in this patient was an MI. Older women have atypical presentations plus the longstanding DM as a CV risk factor..

4. Low Ca, high PTH, low PO4, high ALP

5. Don't know. Not CF, maybe Wiskott aldrich, but that wouldn't change these labs, maybe kartageners but again no lab changes...
Click to expand...
3. Maybe renal osteodystrophy. Low Ca, high PO4, high PTH, normal high ALP.

5. Maybe Digeorge Syndrome. Low Ca, low PO4, low PTH, normal ALP.
 
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25 year old man presents for annual wellness exam. His medical history is significant for occasional "skipped heart beats" under situations of extreme stress, but denies prolonged episodes of palpitations. No significant family history. He denies use of tobacco, alcohol, or illicit drugs. On exam you find a grade 2 early systolic murmur at the left lower sternal border. Remainder of exam is unremarkable. ECG is normal. What is the next best step?

A. Holter monitor
B. Transesophageal echo
C. Transthoracic echo
D. Reassurance
 
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seminoma said:
Pap smear on a 35 year old woman shows CIN III. Terrified, she storms out of your office and you are unable to contact her to discuss prognosis/treatment. She returns 2 years later. At this time you perform another pap smear. What are you most likely to find?

A. Regression of the lesion
B. CIN III
C. CIS
D. Invasive carcinoma without spread to adjacent tissues or mets
E. Mets to obturator and hypogastric nodes
F. Hematogenous lung mets
Click to expand...
CIS? older women are less likely to heal the lesion, plus it's CIN 3
 
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syoung said:
CIS? older women are less likely to heal the lesion, plus it's CIN 3
Click to expand...

It's actually CIN III. It's true that low grade lesions (CIN I) are more likely to regress, but high grade lesions (CINII/III) are more likely to persist than they are to progress to CIS. Kaplan says 60% of high grade lesions persist at the same grade for 2-10 years, with only 10% progressing to CIS/invasive carcinoma.

Pathoma says that CIN I = 66% regress; CIN II 33% regress; CIN III unlikely to regress. Nothing about progression though.
 
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7pkre7K.png


Pink line represents an aromatase inhibitor. Which one is it?
 
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Pap smear shows 100% parabasal cells and is interpreted as normal. How old is this patient?

<21
21-45
46-60
>60
 
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seminoma said:
25 year old man presents for annual wellness exam. His medical history is significant for occasional "skipped heart beats" under situations of extreme stress, but denies prolonged episodes of palpitations. No significant family history. He denies use of tobacco, alcohol, or illicit drugs. On exam you find a grade 2 early systolic murmur at the left lower sternal border. Remainder of exam is unremarkable. ECG is normal. What is the next best step?

A. Holter monitor
B. Transesophageal echo
C. Transthoracic echo
D. Reassurance
Click to expand...
D. Possible functional murmur?
 
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Per original post:

What are the calcium, phosphate, ALP and PTH levels in the following situations:

1) 72-year-old woman with kyphosis and Hx of left hip fracture from prior fall; no Hx of renal pathology or abnormal urinalyses.

2) 60-year-old man with recent R-sided hearing loss; no tinnitus; no vertigo; favorite baseball cap that he's had for years is a bit more snug.

3) 65-year-old woman with 30-year Hx of T2DM; recent pain in left forearm.

4) 44-year-old man; chronic alcoholic; blood pressure taken in ED causes forearm twitching.

5) 15-year-old boy with childhood Hx of recurrrent pneumonia and bronchiolitis; weight and height both 10%tile; patient does not report anything wrong with stools; no recent travel; petechiae on shoulders.

seminoma said:
@Phloston

1. Normal. Ca, PO4, ALP, PTH are normal in osteoporosis. Unless she's being treated.. but then I think the labs would depend on the regimen.

2. Looks like Paget's. So high ALP, everything else normal.

3. No idea. I would say osteoporosis, but they're asymptomatic until a bone breaks. Osteoarthritis won't start in the forearm. Neuropathy won't change the labs. Charcot joint won't be in the forearm. Honestly the first thing I thought of in this patient was an MI. Older women have atypical presentations plus the longstanding DM as a CV risk factor..

4. Low Ca, high PTH, low PO4, high ALP

5. Don't know. Not CF, maybe Wiskott aldrich, but that wouldn't change these labs, maybe kartageners but again no lab changes...
Click to expand...

#1/2 yeah.

#3 = secondary hyperparathyroidism in a patient with chronic renal failure. Bony changes caused by the increased PTH, eg., renal osteodystrophy / osteitis fibrosa cystica.

#4 = hypomagnesemia --> secondary hypoparathyroidism --> low calcium, high phosphate, normal ALP, low PTH

#5 = CF; patients often report nothing wrong with stools; doesn't have to be overt steatorrhea like with giardiasis; fat-soluble vitamin deficiency --> vitamin D deficiency --> low calcium, low phosphate, normal or high ALP, normal or increased PTH
 
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Phloston said:
Per original post:

What are the calcium, phosphate, ALP and PTH levels in the following situations:

1) 72-year-old woman with kyphosis and Hx of left hip fracture from prior fall; no Hx of renal pathology or abnormal urinalyses.

2) 60-year-old man with recent R-sided hearing loss; no tinnitus; no vertigo; favorite baseball cap that he's had for years is a bit more snug.

3) 65-year-old woman with 30-year Hx of T2DM; recent pain in left forearm.

4) 44-year-old man; chronic alcoholic; blood pressure taken in ED causes forearm twitching.

5) 15-year-old boy with childhood Hx of recurrrent pneumonia and bronchiolitis; weight and height both 10%tile; patient does not report anything wrong with stools; no recent travel; petechiae on shoulders.



#1/2 yeah.

#3 = secondary hyperparathyroidism in a patient with chronic renal failure. Bony changes caused by the increased PTH, eg., renal osteodystrophy / osteitis fibrosa cystica.

#4 = hypomagnesemia --> secondary hypoparathyroidism --> low calcium, high phosphate, normal ALP, low PTH

#5 = CF; patients often report nothing wrong with stools; doesn't have to be overt steatorrhea like with giardiasis; fat-soluble vitamin deficiency --> vitamin D deficiency --> low calcium, low phosphate, normal or high ALP, normal or increased PTH
Click to expand...

I'm ok with #5, but how likely is it that a patient with 30 year history of T2DM is going to progress to osteitis fibrosa cystica? Isn't the PTH excess going to get caught way earlier and not become a problem?

Also for #4 how do we determine the extent of the hypomag? I was thinking malnourished/vit D deficiency.
 
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seminoma said:
I'm ok with #5, but how likely is it that a patient with 30 year history of T2DM is going to progress to osteitis fibrosa cystica? Isn't the PTH excess going to get caught way earlier and not become a problem?

Also for #4 how do we determine the extent of the hypomag? I was thinking malnourished/vit D deficiency.
Click to expand...

#3) There aren't any laws in medicine (as you know) about how things present. I've seen patients with very bizarre constellations of symptoms that have stumped internists. The bone pain was just an extra. But the driving point is that diabetes is the most common cause of chronic renal failure. And someone with a 30-year-Hx developing bone symptoms should warrant investigation for renal failure and secondary hyperparathyroidism.

#4) If you sample 100 random people off the street, a lot of them will be vitamin D deficient. But regardless, to get vitamin D deficiency severe and long-term enough to cause symptoms generally requires a pathology apart from just dietary deficiency (e.g., malabsorption). Alcoholics are frequently magnesium deficient.
 
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normally i pretty good with biostat but can't work this out.

Sensitivity is 95%, specificity is 95%. prevalence changes from 20% to 1%.
what will be the change in PPV?
 
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Krasmyc said:
normally i pretty good with biostat but can't work this out.

Sensitivity is 95%, specificity is 95%. prevalence changes from 20% to 1%.
what will be the change in PPV?
Click to expand...

Decrease because PPV is directly proportional to prevalence. NPV would increase because it is inversely proportional to prevalence.
 
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Krasmyc said:
i should have been more specific. they wanted the number. options mentioned were:
15%, 10%, 5%, 1%
Click to expand...
I suck at Biostats but I'd go with 5%.

The PPV in this case is 95% and I multiplied it by the change in prevalence (1/20) to get 4.75%.
 
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seminoma said:
Febuxostat isn't a a purine analogue and its metabolites don't inhibit XO like allopurinols do. IIRC allopurinol = short half life, but its degredation product (catalyzed by XO) has a super long half life == the main effect.
Click to expand...
It works by blocking the molybdenum dependent co-factor for xanthine oxidase.
 
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dfib slim said:
I suck at Biostats but I'd go with 5%.

The PPV in this case is 95% and I multiplied it by the change in prevalence (1/20) to get 4.75%.
Click to expand...

wait how did u get PPV of 95%?

https://onlinecourses.science.psu.edu/stat507/node/71

well i assumed sample size of 1000 and plugged the values in with 20% prevalence. next when u change the prevalence to 1% that would mean dec TP and using this i got 16%

n= 1000
prevalence 20%---> TP: 200 FN: 10 FP 40 TN: 750----> PPV: 83%
prevalence 1%----> TP: 10 FN: 0.5 FP 49 TN 939-----> PPV: 16.9% wtf

this is so messed up
 
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Krasmyc said:
wait how did u get PPV of 95%?

https://onlinecourses.science.psu.edu/stat507/node/71

well i assumed sample size of 1000 and plugged the values in with 20% prevalence. next when u change the prevalence to 1% that would mean dec TP and using this i got 16%

n= 1000
prevalence 20%---> TP: 200 FN: 10 FP 40 TN: 750----> PPV: 83%
prevalence 1%----> TP: 10 FN: 0.5 FP 49 TN 939-----> PPV: 16.9% wtf

this is so messed up
Click to expand...
What was the correct answer?

I set up my 2x2 table like this.
+ -
+ 95 5
- 5 95

TP=95, FN=5, FP=5, TN=95

That gives a sensitivity, specificity, and PPV of 95%

Since the PPV varies directly with the prevalence, and the prevalence decreases from 20% to 1%, I multiplied the PPV by the decrease in prevalence.

Edit: stupid formatting
 
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Krasmyc said:
wait how did u get PPV of 95%?

https://onlinecourses.science.psu.edu/stat507/node/71

well i assumed sample size of 1000 and plugged the values in with 20% prevalence. next when u change the prevalence to 1% that would mean dec TP and using this i got 16%

n= 1000
prevalence 20%---> TP: 200 FN: 10 FP 40 TN: 750----> PPV: 83%
prevalence 1%----> TP: 10 FN: 0.5 FP 49 TN 939-----> PPV: 16.9% wtf

this is so messed up
Click to expand...

Just about what I got as well.

dfib slim said:
What was the correct answer?

I set up my 2x2 table like this.
+ -
+ 95 5
- 5 95

TP=95, FN=5, FP=5, TN=95

That gives a sensitivity, specificity, and PPV of 95%

Since the PPV varies directly with the prevalence, and the prevalence decreases from 20% to 1%, I multiplied the PPV by the decrease in prevalence.

Edit: stupid formatting
Click to expand...

Based on my very basic handle on biostats, I would be willing to bet that PPV is never 95% if prevalence is 1%.
 
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Krasmyc said:
normally i pretty good with biostat but can't work this out.

Sensitivity is 95%, specificity is 95%. prevalence changes from 20% to 1%.
what will be the change in PPV?
Click to expand...

PPV- Would go down? Are you asking for like an exact number?

As a general concept when Prevalence Increases so does PPV and vice versa.

Edit: Didn't read the posts completely before posting. My bad
 
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seminoma said:
Based on my very basic handle on biostats, I would be willing to bet that PPV is never 95% if prevalence is 1%.
Click to expand...
Yeah I was thinking it didn't sound right. Biostats is the bane of my existence. If the question isn't straight forward I just wing it and hope the answer matches up. Sometimes I get it right for the wrong reason, I'll take it.
 
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seminoma said:
Just about what I got as well.



Based on my very basic handle on biostats, I would be willing to bet that PPV is never 95% if prevalence is 1%.
Click to expand...


well i don't know the answer. yikes.

someone sent me the questions (something similar showed up in real thing ) and i wasn't sure so shared with everyone.

check this out
http://www.mas.ncl.ac.uk/~njnsm/medfac/MBBS/handout.pdf

using this answer turns out to be 1%

https://www.medcalc.org/calc/diagnostic_test.php

anyways! this is just screwed up. i will just mark it and move on.
 
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Study was conducted b/w Pancreatic Ca and increase Caffeine intake. R.R of the study is 1.4. On further analysis smoking was carefully corrected in the study showed R.R to be 1.2. Smoking has what sort of effect on the study?
a. confounding b. effect modification
 
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how does the methacholine challenge test for asthma? as in what does acetylcholine stimulation have to do with diagnosing bronchial hyperactivity?
 
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aspiringmd1015 said:
how does the methacholine challenge test for asthma? as in what does acetylcholine stimulation have to do with diagnosing bronchial hyperactivity?
Click to expand...

Bronchial hyper responsiveness is a defining feature of asthma and is a manifestation of exaggerated reversible airway obstruction due to smooth muscle contraction.
in asthma what happens is there is ---> inc Th2---> via IL 5---> inc eosinophil, plus inc in Leukoterine. all these predispose a person to bronchoconstriction with right environmental agent to which person is sensitized.

Anyways so basically there is upregulartion of the receptors in the airway for broncho-constriction. Acetylcholine act via M3 on airways.
Reason why we use methacholine is that in the dosage it is been used, it won't cause bronchoconstriction in normal person but someone whose is hyper responsive to Ach will develop reversible bronchoconstriction, as its effect is short lived.
 
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osteomyelitis: yes osteomyelitis is associated with salmonella in sickle cell, but is staph aureus still the most common cause even in sickle cell?
 
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