Official Step 1 High Yield Concepts Thread

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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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What if I said it's also a potent vasodilator?

Well, my dad told me that back in the day some people took amyl nitrate, aka poppers, before sex. Since it's also an antidote for CN poisoning, I'm guessing this is the one you're thinking about.
 
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Well, my dad told me that back in the day he would see people taking amyl nitrate, aka poppers, before sex. Since it's also an antidote for CN poisoning, I'm guessing this is the one you're thinking about.
Yup, amyl nitrite. And it's still being used. I've transported a few people over the years for syncopal episodes from using it.
 
Yup, amyl nitrite. And it's still being used. I've transported a few people over the years for syncopal episodes from using it.

Didn't know that was still a thing. Hah, I realized that my original post could've been misconstrued. I was trying to say that my dad saw people at the hospital in the same situation as you.
 
Well, my dad told me that back in the day some people took amyl nitrate, aka poppers, before sex. Since it's also an antidote for CN poisoning, I'm guessing this is the one you're thinking about.

I read it somewhere too. It's a part of Cyanide antidote kit = Amyl nitrite, sodium nitrite and sodium thiosulfate
 
amyl nitrite and amyl nitrate are completely different things.

What is amyl nitrate used as an antidote for? I learned about it as a vasodilator, but not as an antidote for anything.
 
Pathogenesis of concentric vs eccentric ventricular hypertrophy?

Concentric = pressure overload. Occurs in response to increased afterload.
Eccentric = volume overload. Occurs because the ventricle gets stretched (excess volume) and also hypertrophies. One thing that was really confusing to me in the beginning of cardio was that dilated hearts still weigh way more than normal hearts because of the eccentric hypertrophy. So even though the walls look really thin, they are actually a lot more dense and therefore weigh more compared to a normal heart. This is true for empty hearts too (it's not because the dilated heart has more volume == is more heavy).

What is the purpose of respiratory epithelium? Where is resistance the highest in the respiratory tree? Where is it the lowest?
 
One thing that was really confusing to me in the beginning of cardio was that dilated hearts still weigh way more than normal hearts because of the eccentric hypertrophy. So even though the walls look really thin, they are actually a lot more dense and therefore weigh more compared to a normal heart. This is true for empty hearts too (it's not because the dilated heart has more volume == is more heavy).
In both cases sarcomeres are added to existing ones in myocytes.
In Concentric Hypertrophy they are added in parallel so the chamber size is reduced ---> difficulty relaxing ---> Diastolic dysfunction.
In Eccentric Hypertrophy they are added in series so the chamber size is increased ---> difficulty contracting (Laplace law) ---> Systolic dysfunction.
 
amyl nitrite and amyl nitrate are completely different things.

What is amyl nitrate used as an antidote for? I learned about it as a vasodilator, but not as an antidote for anything.

They are oxidants to induce methemoglobinenmia in order to bind the cyanide, then the thiosulfate binds the cyanide for excretion in the urine.
 
They are oxidants to induce methemoglobinenmia in order to bind the cyanide, then the thiosulfate binds the cyanide for excretion in the urine.
That's amyl nitrite, not nitrate.

Amyl nitrite is used for both cyanide toxicity and angina.

Amyl nitrate is not used for any medical purposes and is different from "nitrates" such as NTG and isosorbide dinitrate.
 
That's amyl nitrite, not nitrate.

Amyl nitrite is used for both cyanide toxicity and angina.

Amyl nitrate is not used for any medical purposes and is different from "nitrates" such as NTG and isosorbide dinitrate.

Yep. From Katzung.

Amyl nitrite and related nitrites are highly volatile liquids. Amyl nitrite is available in fragile glass ampules packaged in a protective cloth covering. The ampule can be crushed with the fingers, resulting in rapid release of vapors inhalable through the cloth covering. The inhalation route provides very rapid absorp- tion and, like the sublingual route, avoids the hepatic first-pass effect. Because of its unpleasant odor and short duration of action, amyl nitrite is now obsolete for angina.
 
Concentric = pressure overload. Occurs in response to increased afterload.
Eccentric = volume overload. Occurs because the ventricle gets stretched (excess volume) and also hypertrophies. One thing that was really confusing to me in the beginning of cardio was that dilated hearts still weigh way more than normal hearts because of the eccentric hypertrophy. So even though the walls look really thin, they are actually a lot more dense and therefore weigh more compared to a normal heart. This is true for empty hearts too (it's not because the dilated heart has more volume == is more heavy).

What is the purpose of respiratory epithelium? Where is resistance the highest in the respiratory tree? Where is it the lowest?
Purpose is to filter using the ciliary escalator and make mucous. Resistance is highest at the bronchioles and I think lowest at the alveoli.
 
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That's amyl nitrite, not nitrate.

Amyl nitrite is used for both cyanide toxicity and angina.

Amyl nitrate is not used for any medical purposes and is different from "nitrates" such as NTG and isosorbide dinitrate.

Woops, good call. I remember from somewhere that nitrites and nitrates are oxidants causing methemoglobinenmia. I knew nitrites but hadn't heard of nitrates having the same effect until then. Maybe it was a mistake in that source. My bad everyone.
 
Purpose is to filter using the ciliary escalator and make mucous. Resistance is highest at the bronchioles and I think lowest at the alveoli.

Yeah so I think the pressure is highest in medium sized bronchi and lowest in the terminal bronchioles. It's probably even lower in the alveoli, but we learned in physio that the resistance isn't actually measured beyond the terminal bronchioles.
 
In PV, you get itch after taking a hot shower but what's the mechanism behind. I know there is an increase in mast cell and all that release histamine but why would taking a shower trigger this? Just curious ?
 
In PV, you get itch after taking a hot shower but what's the mechanism behind. I know there is an increase in mast cell and all that release histamine but why would taking a shower trigger this? Just curious ?
Temperature induced mast cell degranulation I believe.
 
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yeah its opposite for the circulatory system, Resistance highest in the arterioles, but in the airways its in the larger airways where the resistance is higher
 
Reye's syndrome causes hepatic enceph, FA says aspirin inhibits mitochondrial beta oxidation, so decreased atp and i guess ketone bodies, thus liver fails and build of ammonia that cant be detoxed = enceph?
 
In PV, you get itch after taking a hot shower but what's the mechanism behind. I know there is an increase in mast cell and all that release histamine but why would taking a shower trigger this? Just curious ?
It is due to basophil activation by JAK2 V617F mutation which release histamine. However, platelets also appears to be involved since it is not relieved by antihistamine but aspirin seems to help.
Exact mechanism is not known but activation of dermal mast cells may be involved similar to dermatographism.
 
Recovering heroin addict being treated for tuberculosis develops withdrawal symptoms despite being on usual dose of Methadone ?
 
or, decreased gfr, reduced load to PCT, more % of Na and water reabsorbed in PCT bc of less load, so less aldosterone secreted, less aldo, less K excretion?
 
In what renal structure does urine first flow through and what is the embryonic origin of that structure?
 
One way could be increased uremia, metabolic acidosis, potassium shift.

Thanks that makes sense. I was wondering if there is a more direct cause? Firecracker says "A decrease in GFR results in increased BUN, extracellular potassium and plasma creatinine levels."
 
Thanks that makes sense. I was wondering if there is a more direct cause? Firecracker says "A decrease in GFR results in increased BUN, extracellular potassium and plasma creatinine levels."
Maybe something like hyporeninemic hypoaldosteronism from atrophy of the juxtaglomerular apparatus in CKD?
 
In what renal structure does urine first flow through and what is the embryonic origin of that structure?
Podocytes, intermediate mesoderm (metanephric blastema)

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In which patients is the diphtheria, pertussis, tetanus vaccine contraindicated?
Apparently history of seizure disorder.
I saw that question but found no evidence to back it up. CDC states it's contraindicated in patients with a neuro problem after receiving the first dose and a precaution in patient's with uncontrolled seizure disorder. Doesn't mention contraindication with a controlled seizure disorder.
 
Apparently history of seizure disorder.
I saw that question but found no evidence to back it up. CDC states it's contraindicated in patients with a neuro problem after receiving the first dose and a precaution in patient's with uncontrolled seizure disorder. Doesn't mention contraindication with a controlled seizure disorder.

Yea that question was the first I'd ever heard of that.. Maybe rx is just wrong?
 
What two ways does hypovolemia contribute to metabolic alkalosis (neither directly involves potassium)?
 
What two ways does hypovolemia contribute to metabolic alkalosis (neither directly involves potassium)?
Increased RAAS
1. ATII-->Increase in sodium and hydrogen ion exchanger activity in the PCT.

2. Increase in aldosterone--> Increased hydrogen ion secretion in the alpha intercalated cell.
 
Pathophysiology of saline responsive vs saline unresponsive metabolic alkalosis?

What are some examples and why are some fixed with saline and others aren't.
 
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Pathophysiology of saline responsive vs saline unresponsive metabolic alkalosis?

What are some examples and why are some fixed with saline and others aren't.
Metabolic acidosis associated with volume loss and K+ shift are saline responsive (e.g. DKA) as compared to saline unresponsive metabolic alkalosis e.g. Conn syndrome where aldosterone is continuously trashing K+ & H+, So in Conn only an aldosterone antagonist will help.
 
Hey guys, quick questions...thanks!

1.) Meningitis with a strictly lymphocytes (this was the only part of CSF profile provided with faint AFP staining) in a child of a farmworker? My hunch is viral, but if the only options were bacterial (including Tb, listeria, strep pneumo)....would it be Tb since Tb/fungal have lymphocytes?

2.) Infant child comes in....doctor says initial DNR but parents refuse and so ventilation is started...few days later parents realize condition is not improving and decided to withdraw care...do you continue with the vent or follow parents wishes or consult ethics committee?

3.) Heavy menstrual bleeding in a child and her mom (both african american). What would you be most concerned about on labs? Choices came down to ultimately vwf def and Fe-def anemia...I chose vwF def because of the family history.

4.) Bilateral abdominal masses in an infant who pees a ton...question asked for a diagnosis. My initial hunch was ARPKD but this was not a choice. I think I picked nephrogenic diabetis insipidus...not sure.

5.) Stroke patient comes in...really not cooperating with hospital staff (doesn't appear to be delirium or dementia) and 4 days in says wants to be DNR. Family says patient never expressed such wishes in past and basically opposes DNR. Who do you listen to? This one was tricky because I went with the stroke patient indeed having decision making capacity (I didn't equate stroke with loss of decision making capacity) and listen to the patient. Ideally, I would've went with something along the lines of re-assess patient and his/her decision but this was not an option.

6.) Rando genetics question in a CFTR patient who had a genotype of I507/F508 and the phenotype of cystic fibrosis

In his family tree (which depicted genotypes), he got the I507 allele from his mom's side but there was NO F508 (either carrier or disease) in the paternal side. Answers had crazy choices: imprinting, uniparental disomy, heterozygous disomy, and reactivation of a silenced gene. I think I picked the reactivation of a silenced gene. I was looking for mutation or mosaicism but that was not there.

7.) Loose Diarrhea/diffuse abdominal pain in a foreigner who didn't drink water but did drink some frozen fruit juice. Choices were your classic enteric G(-) bacteria: Camplyobacter jejuni, E. coli, salmonella.

I think I went with E. coli- seemed the most common since the diarrhea was non-bloody.

8.) Someone with gastritis with numerous RF...which one contributes the most- smoking, stress, hot liquids, tynenol use?

9.) Child who becomes hypoglycemia/has baseline hypoglycemia immediately 30 minafter a meal but becomes normoglycemia immediately after eating sugars/taking glucagon. Choices were glycogen storage disorder, insulinoma, brush border enzyme deficiency. I think I went with insulinoma since insulin would spike after a meal and also remain elevated at baseline.

10.) Untrained athlete who starts feeling dizzy 5 miles into a 50 mile bike ride in hot 100 degree+ and high humid temps....if he had trained should he have done that would've been most beneficial? (I think the choices were like drink tons of fluid, change core-body temp)...I went with the try to affect core-body temp, I guess if you lower it, you sweat better (but in retrospect I think that's wrong since the conditions are very humid and sweating is ineffective)?

11.) What is your most important cooling mechanism of training in low humid, hot temperatures? Radiation, convection, evaporative cooling (I think I picked this one).

12.) Someone with a rash who goes out in the woods...sounds like contact dermatitis (>2d)...question asked biopsy features....I think I went with spongiosis since I saw this in UWorld

13.) In a Pneumothorax...what is increased? Alveolar dead space (went with this one) or pulmonary vascular resistance? The latter I felt would've been more common in a PE but I guess my mind was boggling with the concept of reactive vasoconstriction.
 
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