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

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Kind of late to be asking about this, but can someone give an example of "step-wise" decline in vascular dementia? How would that be described in a vignette?
 
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seminoma said:
Kind of late to be asking about this, but can someone give an example of "step-wise" decline in vascular dementia? How would that be described in a vignette?
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A 70-year-old woman came to the clinic with her son for assessment of her cognitive decline. The son is concerned about her short-term memory problems for the past 10 months. Patient had a fall 10 months ago; after that fall, she started to ask the same questions over and over. Patient had another fall 4 months ago and also an episode of dizziness 2 months ago. With each of these incidents, her son noticed further decline in cognition. Recently, her son noticed that she has become a bit more suspicious of her daughter-in-law and has been hoarding things. She has lost interest in her day-to-day activities and forgets to include the right ingredients when cooking. Family has to remind her to take her medications, and her son is helping with the management of her finances.

The patient has h/o hypertension, diabetes, coronary artery disease, osteoarthritis, and osteoporosis.
 
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In the davenport diagram, why does (point D) uncompensated metabolic alkalosis, with compensation lead to a higher bicarb level with the ph going down(point E). Is it because it mostly occurs in chronic conditions so the bicarb will be increased?
 
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Alright guys tell me if I have this right or if I am missing something... So with carboxyhemoglobin, you have CO strongly binding to Hb. At low levels, you actually get increased O2 affinity for Hb and your % saturation will be slightly higher than normal, but then after you increased the CO enough, it will dominate over O2 and you will have decreased %saturation. However, there is a left shift in the oxygen dissociation curve and that is explained by the increased affinity Hb has for O2 when bound to CO? Confusing but trying to wrap my head around why you get decreased %sat but left-shift

(the graph I reference for low CO causing increased % saturation is on p. 604 of FA 2015)
 
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decreased saturation BC CO is bound to HB, so if CO is bound(its a competitive inhibitor) that takes up spots for 02 to bind, but at the same time increasing the affinity of the remaining spots for 02, thus left shifting the curve
 
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seminoma said:
M3 (promyelocytic), M5 (monocytic), and M7(megakaryocytic) are in Pathoma. Others I don't know.
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M3--> promyelocytic and usually presents with DIC and is treated with Vitamin A
M5--> Monocytic and presents with gum infiltration
M7: Increased incidence in Down and children


faisal 2000 said:
what is hypokalemic periodic paralysis ?
Click to expand...
 
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faisal 2000 said:
M3--> promyelocytic and usually presents with DIC and is treated with Vitamin A
M5--> Monocytic and presents with gum infiltration
M7: Increased incidence in Down and children
Click to expand...

Before age 5 for M7. Or maybe it's after age 5. Can't remember, but Sattar says it's important.
 
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sattar says before for AML M7, and after age 5 for ALL. Also, the all one makes sense bc the transolcation is involving the 21 chromosome, t(12;21)
 
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seminoma, i inboxed you(please get back to me when you can!) also, any idea where i can get a concise understanding of some of the bedside maneuver effects on heart sounds? some are obvious but some dont make sense to me
 
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faisal 2000 said:
what is the mechanism of hypokalemia in renal tubular acidosis ?
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RTA 1 -> decreased functioning of alpha intercalated cells that normally create and excrete H+ and resorb the bicarb they make via carbonic anhydrase -> decreased H+ in tubular lumen -> K+ is drawn more strongly into the lumen to fix the electronegative difference -> hypokalemia and metabolic acidosis

RTA 2 -> PCT cells decrease function (Wilson's disease causing Fanconi Syndrome, or acetazolamide) -> tons more Na/K/bicarb etc in tubular lumen than would normally be -> Na is preferentially saved in the collecting tubules at the expense of K+ -> hypokalemia and metabolic acidosis

RTA 4 -> decreased aldosterone or aldosterone insensitivity (adrenal failure, Legionaire's disease) -> hyperkalemia and metabolic acidosis
 
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A/c to RR path, the increased filitered hc03 binds to K causings its excreition, but either way, just know hypokalemia with a ph of <5.5(urine)
 
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dartmed said:
How does obstructive sleep apnea cause an increase in pulse pressure and a pulsus parodoxus? Thanks!!
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Pulmonary hypertension -> right heart experiences hypertension -> pressure difference between left and right ventricles becomes much smaller -> interventricular septum bulges into the left heart during inspiration when there is extra blood entering the right heart -> left side of heart experiences outflow obstruction during inspiration = pulsus paradoxus and narrowed pulse pressure
 
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was listening to goljan, and he mentioned that dipyridamole effects thrombaxanse synthase and aspirin only works on cox, but in FA it doesnt have anything about that, can anyone clear this up?
 
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how Vit A toxicity can cause pseudotumor cerebri ?
how can we differentiate between pseudotumor cerebri and cluster headache ?
 
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faisal 2000 said:
how Vit A toxicity can cause pseudotumor cerebri ?
how can we differentiate between pseudotumor cerebri and cluster headache ?
Click to expand...

Pseudotumor cerebri: seen mostly in women of child bearing age. PE will show papilledema, and abducens nerve palsy may be present. Patient will complain of severe headache, tinnitus, and visual disturbances. You'll likely see it in the context of pregnancy or an endocrine disturbance.

Cluster headache: more commonly seen in males > females (6:1). Can be precipitated by alcohol, tobacco or stress. The headache will be unilateral/periorbital, described as a sudden stabbing pain, and will be brief and episodic occuring in a particular time of the day. It can be accompanied by rhinorrhea, ipsilateral ptosis, ipsilateral lacrimation.
 
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aspiringmd1015 said:
was listening to goljan, and he mentioned that dipyridamole effects thrombaxanse synthase and aspirin only works on cox, but in FA it doesnt have anything about that, can anyone clear this up?
Click to expand...

Dipyridamole inhibits platelet PDE leading to an increase in cAMP (anti-aggregatory), inhibits thromboxane synthase, and inhibits adenosine deaminase.

Aspirin prevents the formation of PGH2 by inhibiting COX-1, so PGH2 ----thromboxane synthase--> thromboxane A2 reaction can't move forward, but it doesn't directly inhibit thromboxane synthase.
 
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psylocke said:
Dipyridamole inhibits platelet PDE leading to an increase in cAMP (anti-aggregatory), inhibits thromboxane synthase, and inhibits adenosine deaminase.

Aspirin prevents the formation of PGH2 by inhibiting COX-1, so PGH2 ----thromboxane synthase--> thromboxane A2 reaction can't move forward, but it doesn't directly inhibit thromboxane synthase.
Click to expand...
thanks, is there any source i can read this from?
 
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faisal 2000 said:
how Vit A toxicity can cause pseudotumor cerebri ?
how can we differentiate between pseudotumor cerebri and cluster headache ?
Click to expand...

We actually had a discussion about this awhile back. The reason is that the vitamin A destroys the arachnoid granulations resulting in fluid backup in the ventricles and subsequent intracranial pressure increase. Cluster headache would pretty much be a giveaway and would be higher on your differential because pseudotumor cerebri, also known as idiopathic intracranial hypertension (IIH), is idiopathic meaning we really don't understand it fully and thus it is usually a diagnosis of exclusion. Cluster headaches will have characteristic giveaways like unilateral headache, severe pain behind the eye socket, and is probably going to occur in a male. If it just doesn't fit those symptoms and there is some kind of risk factor for IIH then you would go that route in your diagnosis. IIH also normally occurs in women of childbearing age that are overweight, so sex alone can help you distinguish between IIH and cluster headaches.
 
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Should we knwo about the cerebellum in detail? or is the half a page part in FA enough? i read it from kaplan in extreme detail, not sure how much time i should take on it.
 
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aspiringmd1015 said:
Should we knwo about the cerebellum in detail? or is the half a page part in FA enough? i read it from kaplan in extreme detail, not sure how much time i should take on it.
Click to expand...

I haven't gotten anything on it at all in UWorld so probably don't need to know much other than what FA has. Even that might be more than we need lol... They will probably test us mainly on tumors and ataxia, probably not much anatomy stuff
 
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aspiringmd1015 said:
Should we knwo about the cerebellum in detail? or is the half a page part in FA enough? i read it from kaplan in extreme detail, not sure how much time i should take on it.
Click to expand...

My guess would be ipsilateral ataxia is the most important thing about the cerebellum for step 1. That and the fact that a positive romberg is typically not a cerebellar sign.
 
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Alright can someone tie together this biochem for me...

I see two diagrams for THF in first aid and each time Pathoma or FA talks about THF I always try and go back to look at the diagrams, and each time I get frustrated because I am unsure of how to correlate the two.

One shows: THF-methyl + dUMP -> dUTP + DHF (pyrimidine synthesis)

The other shows: THF-methyl + homocysteine -> methionine (this pathway shows B12 involved)

So how do these two pathways relate? I see that obviously the common denominator is THF-methyl donating methyl groups... so are these two separate pathways or am I missing some correlation ?? Its just confusing me
 
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pathologyDO said:
Alright can someone tie together this biochem for me...

I see two diagrams for THF in first aid and each time Pathoma or FA talks about THF I always try and go back to look at the diagrams, and each time I get frustrated because I am unsure of how to correlate the two.

One shows: THF-methyl + dUMP -> dUTP + DHF (pyrimidine synthesis)

The other shows: THF-methyl + homocysteine -> methionine (this pathway shows B12 involved)

So how do these two pathways relate? I see that obviously the common denominator is THF-methyl donating methyl groups... so are these two separate pathways or am I missing some correlation ?? Its just confusing me
Click to expand...

Don't confuse methyl-THF with methylene-THF. Methyl-THF is used in methionine synthesis. Methylene-THF is used in pyrimidine synthesis.
 
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pathologyDO said:
OK now you've got me really messed up in the head. Going to the ER to check into psych ward, brb
Click to expand...

1ycyBCP.png


As far as I know FA differentiates between methylene and methyl. If it doesn't, then it should have.
 
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so methyl-thf being the trapped or storage form, has to give its methyl group to b12 and then subsequently to homocysteine to form methionine, and methylene is the methyl group thats added to UMP to make TMP. epic.
 
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in pseudotumor cerebri, is it the direct effect of increased ICP thats lesions abducens? or is there some other mechanism behind it(ie some kind of herniation)
 
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for ASA occlusion, can anyone explain what theyre trying to say by saying adamkiewicz supplies below T8, i wiki'd the artery, and was way too much crap to read.
 
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aspiringmd1015 said:
for ASA occlusion, can anyone explain what theyre trying to say by saying adamkiewicz supplies below T8, i wiki'd the artery, and was way too much crap to read.
Click to expand...

Basically there is a watershed region where the artery of adamkiewicz meets the ASA, and so the T4-T8 region between the two is most vulnerable. This is known as ASA syndrome and leads to bilateral loss of pain and temperature (spinothalamic tract), bilateral weakness (lateral corticospinal tract) with preservation of fine touch, proprioception, and vibration (dorsal column)
 
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okay cool, btw i was watching sketchymciro, and they said the only RNA virus to replicate within the nucleus are the orthomyxoviridiae, i thought HIV did too, and also read it in FA, the RT activity is definitely in the cytoplasm, but the integration into the host dna and all that is in the nucleus. So whats the deal with that?
 
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Antibody changes in experimental anisakiasis were observed in 10 rabbits which were infected each with 10 Anisakis simplex larvae. The sera were collected before and on the 6th to the 95th day after the infection. Using crude saline extract of Anisakis larvae as antigen, specific IgM and IgG antibody levels were observed by ELISA and SDS-polyacrylamide gel electrophoresis/immunoblot. Levels of specific-IgM antibody were elevated from the 6th day, reached their peaks on the 11th day after the infection, and dropped thereafter. Serum levels of IgG antibody increased from the 6th day and reached their peak on the 26th day after the infection, and decreased gradually thereafter. When SDS-PAGE of the crude extract was done, at least forty-one SDS-polypeptide bands were recognized. Of them, IgM antibody reacted mainly to the bands of 168, 95, 74, 64, 51, 47 and 34 kDa while IgG antibody reacted strongly to 168, 92, 85, 64, 58, 52, 42 and 40 kDa bands. The crude extract showed negligible cross reactions with sera of other parasitic diseases and normal control. Number of J chain in an IgM pentamer?
a) 1
b) 2
c) 3
d) 4
e) 5
 
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