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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What's the difference between Paroxysmal Supraventricular Tachycardia, Paroxysmal Atrial Tachycardia & Re-entrant tachycardia ?
 
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33 year old has a minor operation where he is fully anesthetized. On completion, he seems to regain consciousness but still be paralyzed.

1) Why? (I can think of two possible reasons, one being much more likely than the other)
2) What are two ways to treat it?
3) Which of those treatments don't work if the patient didn't have the original complication?
 
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stepone2015 said:
Thought it was an ectopic pacemaker?
Click to expand...
Sure, the ectopic pacemaker activity essentially arises from the extension of myocardium in the pulmonary veins.

In our cardio module, I clearly remember our lecturer mentioning possibilities of other foci but pulmonary veins being the most common.
 
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psylocke said:
Sure, the ectopic pacemaker activity essentially arises from the extension of myocardium in the pulmonary veins.

In our cardio module, I clearly remember our lecturer mentioning possibilities of other foci but pulmonary veins being the most common.
Click to expand...

That's nuts, didn't know that, thanks.
 
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with autoregulatory BP mechanisms, it states that the renal blood pressure and flow is autoregulated between 90 and 180. So what happens when the BP falls oustide of these parameters? as in above 180, or below 90?
 
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faisal 2000 said:
sjogren syndrome is autoimmune disease characterized by lymphocytic infiltration of lacrimal and salivary gland causing dry mouth and eyes.normally saliva is rich in bicarbonate which neutralize acid in esophagus, so in sjogren syndrome absence of saliva will leads to esophagus damage with even GERD .
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scleroderma(diffuse and localized)
 
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faisal 2000 said:
how does obesity cause hypopituitarism ???
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I suppose you are refering to the association of obesity with empty sella syndrome where, if I recall correctly, the subarachnoid space herniates into the sella and displaces /compresses the pituitary gland potentially resulting in hypopituitarism. I never however really understood the mechanism of obesity causing empty sella or really the syndrome itself. Please expand on my answer as I would not mind to learn more about it (assuming I answered correctly).
 
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What associated symptoms/findings (non-thyroid) could be found in a patient with enlarged thyroid and low TSH/T3 where biopsy shows mainly fibrous replacement of the thyroid? What serum protein would in that case be elevated?

Hope Im not beeing to vague here.
 
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What is the MOA (action and serotonin receptor subtype) of the treatments to these conditions:
- Patient with n/v after chemotherapy?
- Patient with unilateral throbbing headache with photophobia lasting 24 hrs?
- Patient with GAD that is intolerant to SSRIs/SNRIs and has prior benzodiazepine abuse?
- Older depressed lady that also has insomnia and appear malnourished?
 
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Radiolucent said:
What associated symptoms/findings (non-thyroid) could be found in a patient with enlarged thyroid and low TSH/T3 where biopsy shows mainly fibrous replacement of the thyroid? What serum protein would in that case be elevated?

Hope Im not beeing to vague here.
Click to expand...
Riedel Sclerosing Thyroiditis
IgG4 would be increased. I think autoimmune pancreatitis and retroperitoneal Fibrosis or something like that.
I remember something also about a Polish sounding name starting with M (don't want to butcher the spelling) maybe it was salivary gland involvement or something.
 
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Radiolucent said:
What is the MOA (action and serotonin receptor subtype) of the treatments to these conditions:
- Patient with n/v after chemotherapy?
- Patient with unilateral throbbing headache with photophobia lasting 24 hrs?
- Patient with GAD that is intolerant to SSRIs/SNRIs and has prior benzodiazepine abuse?
- Older depressed lady that also has insomnia and appear malnourished?
Click to expand...
Ondansetron 5HT3 antagonist (I think it might act on vagus not sure exactly).
Sumatriptan or other Triptans 5-HT 1BD agonist. Decreases release of vasoactive peptides.
Buspirone activates 5HT1A receptor (not sure). Also increases dopamine and NE levels.
Mirtazapine alpha 2 blocker but also I think is involved with Serotonin receptors but not sure which ones. Helps in this case by causing weight gain and sedation.
 
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Mirtazapine:
1. 5-HT2A receptor antagonist ---> Antidepressant (but no sexual side effects)
2. α2-adrenergic receptor antagonist ---> Antidepressant, increased α2 stimulation --> NE synthesis and release from locus ceruleus neurons ---> 5-HT release from raphe neurons
3. 5-HT 1A receptor agonist ---> Anxiolytic
4. H1 receptor inverse agonist ---> increases appetite (along with 5-HT 2C antagonism), sedative effect.
5. 5-HT3 receptor antagonist ---> antiemetic
 
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Kingella said:
Riedel Sclerosing Thyroiditis
IgG4 would be increased. I think autoimmune pancreatitis and retroperitoneal Fibrosis or something like that.
I remember something also about a Polish sounding name starting with M (don't want to butcher the spelling) maybe it was salivary gland involvement or something.
Click to expand...
Precisely; Riedels thyroiditis iss associated with the IgG4 related disorders which contain, among others, autoimmune pancreatitis, aortitis and retroperitoneal fibrosis. Mikuliczs disease which you almost mentioned (yes, he was Polish) is when the salivary glands are involved.
Basically IgG4 related diseases are inflammatory-fibrous diseases in which you can see IgG4 plasma cell infiltrate histologically.

Kingella said:
Ondansetron 5HT3 antagonist (I think it might act on vagus not sure exactly).
Sumatriptan or other Triptans 5-HT 1BD agonist. Decreases release of vasoactive peptides.
Buspirone activates 5HT1A receptor (not sure). Also increases dopamine and NE levels.
Mirtazapine alpha 2 blocker but also I think is involved with Serotonin receptors but not sure which ones. Helps in this case by causing weight gain and sedation.
Click to expand...

Transposony said:
Mirtazapine:
1. 5-HT2 (especially 2A) receptor antagonist ---> Antidepressant
2. α2-adrenergic receptor antagonist ---> Antidepressant
3. H1 receptor inverse agonist ---> increases appetite, sedative/hypnotic effects.
4. 5-HT3 receptor antagonist ---> antiemetic
Click to expand...

Good job guys. Those 5-HT receptors can be easy to mix up and therefore it can be good to compare them side by side.
 
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for fanconis anemia, some causes listed cause liver disease(wilsons glycogen storage diseases) so does the fanconi's then develop bc of hepatorenal syndrome?
 
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MOA of:

1) Amiodarone (also, mention the toxicities)
2) Methyldopa (and name one or two side-effects)
3) Levodopa/carbidopa (be specific how these two work together)
4) Lidocaine (also, what happens if injected in a vein)
5) Propafenone
6) Valproic acid (also, #1 Tx for what)
7) Phenytoin (also, what vitamin deficiency does this one cause)
8) Carbamazepine (also, #1 Tx for what)
9) Topiramate
10) Lamotrogine (has a toxicity not unique to this drug, but USMLE obsesses over it for lamotrogine)
11) Acyclovir (also name major toxicity)
12) Fibrates (also name three toxicities)
13) Phenoxybenzamine vs phentolamine (be specific, and also describe the V vs [substrate] curve changes)
14) Statins (what will this do to a V vs [substrate] curve; also, name two toxicities)
15) What is the main effect of niacin? (and name three side-effects; based on these, niacin is therefore contraindicated in which two conditions)
 
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Phloston said:
MOA of:

1) Amiodarone (also, mention the toxicities)
2) Methyldopa (and name one or two side-effects)
3) Levodopa/carbidopa (be specific how these two work together)
4) Lidocaine (also, what happens if injected in a vein)
5) Propafenone
6) Valproic acid (also, #1 Tx for what)
7) Phenytoin (also, what vitamin deficiency does this one cause)
8) Carbamazepine (also, #1 Tx for what)
9) Topiramate
10) Lamotrogine (has a toxicity not unique to this drug, but USMLE obsesses over it for lamotrogine)
11) Acyclovir (also name major toxicity)
12) Fibrates (also name three toxicities)
13) Phenoxybenzamine vs phentolamine (be specific, and also describe the V vs [substrate] curve changes)
14) Statins (what will this do to a V vs [substrate] curve; also, name two toxicities)
15) What is the main effect of niacin? (and name three side-effects; based on these, niacin is therefore contraindicated in which two conditions)
Click to expand...

I´ll give it a try:
1)K+ channel blocker --> prolongs action potential and ERP in myocardium. Used for most arrythmias. Toxicities include hypo/hyperthyroidism (contains iodine), hepatotoxicity, pulmonary fibrosis. Photosensitivity and blue discoloration/deposition in skin/cornea. Like all the antiarrythmics it can cause arrythmias. Has a very long t½. I´m sure theres a lot more here but those are the ones I remember.

2) a2 agonist --> centrally acting to reduce bp. Can clasically be used in pregnancy --> tightly protein bound --> acts as hapten --> hemolytic anemia /drug induced SLE.

3)LDOPA gets converted to dopamine by DOPA decarboxylase (B6 dependant). Carbidopa is a DOPA decarboxylase inhibitor which inhibits peripheral conversion and therefore reducing peripheral side effects (arrythmias, n/v) and increasing availability centrally.

6) Inactivates Na+ channel, inhibits GABA deaminase --> increases GABA (inhibitory neurotransmitter). Used for seizures (incl abscence and myoclonic), bipolar disorder.

8) Inactivates Na+ channels. Used for seizures (mainly partial), 1st line for trigeminal neuralgia.

10) Blocks voltage gated Na+ channels. The boards seem to love Steven-Johnson syndrome here.

14) Mainly inhibits HMG-CoA reductase decreasing formed cholesterol, also decreasing VLDL, upregulation of LDL receptors, and cardioprotective pleiotropic effects. I guess it is a competitive inhibitor so Vmax will stay the same Km increases (not sure if that is what you ment). Hepatotoxic and myotoxic especially when combined with fibrates.

Those are the ones I have time to answer right now, I´ll leave the rest to you guys.
 
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in alport syndrome, you get glomerular bleeding with hematura, is this due to the physical aspect of the immune complexes being deposited in the mesangium? bc with the other nephritic syndromes you get glomerular bleeding and inflammation bc usually IgG/M is being deposited which can activate the complement, but in this case igA cannot activate the complement, soo...?
 
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aspiringmd1015 said:
in alport syndrome, you get glomerular bleeding with hematura, is this due to the physical aspect of the immune complexes being deposited in the mesangium? bc with the other nephritic syndromes you get glomerular bleeding and inflammation bc usually IgG/M is being deposited which can activate the complement, but in this case igA cannot activate the complement, soo...?
Click to expand...

Nephritic vs nephrotic is defined clinically and based off labs (hematuria, amount of proteinuria etc). The actual cause of each is irrelevant. Alport is a nephritic syndrome because the basement membrane in the kidney (among other places) doesn't work properly. It lets in blood and small amounts of protein just like other nephritic diseases. There is no inflammation/Ig/complement systems involved to my knowledge.
 
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Maybe I'm wrong, but I thought all of those were to define the exact cause of each nephritic or nephrotic syndrome. For example, if a patient comes in and has 4 g of protein in their urine without any blood, you've narrowed down your spectrum of possible diseases to various nephrotic syndromes. You then do the biopsy/EM/IF and determine what the cause was - ie minimal change disease.
 
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anyone? sorry, i know i have a lot of questions, but nothing sticks in my brain unless the concept is crystal clear. Also with the different type of anions that increase the anion gap in MA, are we suppose to know the mechanism?
 
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Kingella said:
Saw palmetto (5 alpha red inhibitor)-I think it's been proven to actually not work.
I think yohimbine is Ed treatment although I could be wrong.
Click to expand...

I know next to nothing about the actual uses of yohimbine but isn't it an alpha-2 antagonist? Theoretically, wouldn't yohimbine cause sympathetic overactivity and make BPH worse (alpha-1A stimulation on smooth muscle).
 
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aspiringmd1015 said:
defined clinically? what about all of the EM findings, IF findings, and biopsy findings?
Click to expand...

>3.5 g protein/day without blood or RBC casts -->nephritic
blood and RBC casts with <3.5g protein/day --> nephrotic
>3.5 g protein/day with blood and RBC casts -->nephritic/nephrotic (usually an SLE patient with diffuse proliferative/membranoproliferative)

These are the definitions. EM, IF, and ANCA and biopsy findings nail down particular syndromes.

IF:
  • granular-->type III hypersensitivity--> can be quite a few things
  • linear-->type II hypersensitivity-->almost always Goodpastures
  • IgA-->IgA nephropathy
    • Kid with abdominal pain, arthritis, and "palpable skin lesions" (purpura) after a recent viral illness-->HSP
    • Teenage male (prototypically) with coca-cola urine after a viral illness-->berger
EM:
  • Effacement of podocyte foot processes-->minimal change disease or FSGS
    • -->differentiate with LM findings and presentation
      • Child+no LM abnormality-->minimal change disease
        • this also tends to be selective proteinuria (i.e. albumin)
      • LM abnormalities that affect only parts of some glomeruli-->FSGS
  • Thin basement membrane
  • Alport
  • Deposits
    • Subendothelial
      • MPGN I
        • also associated with "tram-tracking" on LM
    • Intramembranous
      • MPGN II
    • Subepithelial
      • PSGN or membranous
ANCA:
  • pauci-immune
  • c-ANCA/anti-PR3
    • Wegener's Granulomatosis (or if you don't like giving credit to a Nazi, granulomatosis with polyangiitis)
  • p-ANCA/anti-MPO
    • Microscopic polyangiitis (Churg-Strauss does not typically involve the kidney

This list is not comprehensive, but I did the best I could.
 
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lol you really didnt have to do that, all that is pretty much given, but thanks anywyas. What i meant was how does igA neprhopathy cause damage to leak protein and rbcs? bc theres no complement being activated, is it just the physical presence of an immune complex being there?
 
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sloop you seem pretty good on concepts, where could i find all the ideologies behind the causes of Metabolic acidosis?(sufficient for step 1 purposes only)
 
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aspiringmd1015 said:
lol you really didnt have to do that, all that is pretty much given, but thanks anywyas. What i meant was how does igA neprhopathy cause damage to leak protein and rbcs? bc theres no complement being activated, is it just the physical presence of an immune complex being there?
Click to expand...

Not exactly sure. IgA nephropathy does cause some amount of mesangial change/proliferation, although it is not consistently seen. I doubt anybody is going to test you on that detail, but it's a good question.

aspiringmd1015 said:
sloop you seem pretty good on concepts, where could i find all the ideologies behind the causes of Metabolic acidosis?(sufficient for step 1 purposes only)
Click to expand...

I don't know of a particularly good resource. I think I just learned it all from class resources as I was studying.

In any case, I can try to make it simple:

Metabolic acidosis can happen basically two ways: you're ingesting/generating acid or you're losing base (or both).

General schematic is look at your pH and see that you're acidemic. Then you see CO2 is low and you know it's metabolic (this part I presume you know).

Next, calculate the anion gap (normal 10). If it's high-->MUDPILES (ingestions: there is an acid that doesn't normally exist in the body generating a non-accounted for anion)

If it's normal, you're either losing bicarb or retaining acid. Next step is urine anion gap ((Na+K)-(HCO3+Cl)). Negative is neGUTive-->losing HCO3 in the gut. Usually this means diarrhea. If it's positive, you have an RTA. (Type I Distal, Type II proximal, Type IV aldosterone insensitive). Serum potassium goes up as you go up--> hypokalemic, hypokalemic, hyperkalemic. If you see phosphate abnormalities, it's the Fanconi form of Type II, usually caused by drugs like tenofovir or tetracyclines.

I wish I had a resource I could refer you to other than First Aid. Maybe you could review your school's notes on the subject if you're really weak on it?

In any case, this should get you through the majority of acid base questions, I think, unless they ask you about delta-delta gap and combined disorders. I think those are probably low yield though.
 
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i just looked in goljan, looks like he has some explanations of it, will look at it from there. Thanks for the help by the way, i may not be as smart, but im eager as heck to learn. Could you explain the K findings in distal proximal? type 4 makes sense bc of aldo not working.
 
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nvm, i understand proximals too, its obvious. Fanconi-cant absorb anything, and CA inhibitors- aldosterone working to compensate for lost volume
 
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with a negative urine anion gap, that means you have an increased amount of nh4 in the urine right? so that correlates with decreased hc03 levels?
 
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Phloston said:
MOA of:
11) Acyclovir (also name major toxicity)
Click to expand...
it inhibits viral DNA polymerase. it causes nausea, vomiting, diarrhea and/or headache, hallucination,agitation, vertigo, artheralgia, and hepatitis.

Phloston said:
MOA of:
15) What is the main effect of niacin? (and name three side-effects; based on these, niacin is therefore contraindicated in which two conditions)
Click to expand...
niacin reducing total cholesterol, triglycerides, VLDL, LDL, and increasing HDL. side effects are Flushing, hyperglycemia, hyperuricemia, upper GIT distress, hepatotoxicity, so niacin contraindicated in Chronic liver disease & hyperuricemia,DM

Phloston said:
MOA of:
5) Propafenone
Click to expand...
Propafenon Blocks Na+ channels . it is Anti-arrhythmic drug

Phloston said:
MOA of:
12) Fibrates (also name three toxicities)
Click to expand...
Fibrates are agonists of the PPAR-α receptor (peroxisome proliferator-activated receptors) The PPARs are a class of intracellular receptors that modulate carbohydrate and fat metabolism and adipose tissue differentiation., in muscle, liver, and other tissues. Activation of PPAR-α signaling results in:
1)Increased β-oxidation in the liver
2)Decreased hepatic triglyceride secretion
3)increased lipoprotein lipase activity, and thus increased VLDL clearance
4) increased HDL
its side effects are muscle pain with CPK elevation, stomach upset, fibrates increase the cholesterol content of bile, so they may increase the risk for gallstones.
fibrate contraindicated in Hepatic\renal dysfunction
 
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