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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Transposony said:
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
Click to expand...
Lesson learned, read last sentence first lol
 
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w/marcus gunn pupil, just saw a questoin with the lesion in the optic tract thus the lesion is contralateral to the eye being effected, but if the lesion was in the optic nerve itd be ipsilateral correct?
 
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Identify 1-12 structures.
 

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faisal 2000 said:
how can I differentiate b\w vit E deficiency and vit B12 according to peripheral neuropathy symptoms ?
Click to expand...

Its really not gunna be much different I don't think in terms of symptoms, they are gunna probably go after your understanding of diagnostic workup, e.g. increased MMA and megaloblastic anemia in B12 deficiency but not in E
 
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little confused about thiazide diuretics..I read in two different sources that 1) it doesnt effect your medullar osmotic gradient, so you can still reabsorb free water via ADH and are more prone to lower serum Na, whereas i also read that their use in nephro DI, by preventing free water from forming by blocking the na/cl channel, it keeps electrolytes with your water hence, no free water, so not really sure. I think the first idea was in UW, and second was in kaplan pharm.
 
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aspiringmd1015 said:
little confused about thiazide diuretics..I read in two different sources that 1) it doesnt effect your medullar osmotic gradient, so you can still reabsorb free water via ADH and are more prone to lower serum Na, whereas i also read that their use in nephro DI, by preventing free water from forming by blocking the na/cl channel, it keeps electrolytes with your water hence, no free water, so not really sure. I think the first idea was in UW, and second was in kaplan pharm.
Click to expand...

Majority of free water formation and majority of medullary gradient maintenance occurs in the TAL. Some free water formation occurs in the DCT. Both of the things in your post are correct.
 
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but for example, their use in nephro DI, it wouldnt allow free water formation, thus ADH wouldnt work, so that would negate the first concept
 
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also w/PTH, does it work directly by p04'ing the luminal Ca+ channel, or on the Na/Ca2+ transorter on the basolateral membrane. FA and Kaplan have different things. FA says the basolateral pump, Raymon from Kaplan said luminal. Confused. Hate being confused.
 
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aspiringmd1015 said:
but for example, their use in nephro DI, it wouldnt allow free water formation, thus ADH wouldnt work, so that would negate the first concept
Click to expand...

Like I said, the majority of free water is formed in the TAL. Thiazides don't work in the TAL.

I guess I don't follow what you're getting at.
 
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seminoma said:
Do you know why the "brown tumors" form?
Click to expand...

My understanding is that the brown tumors form as a result of primary hyperparathyroidism, where the osteoblasts are working overtime to increase resorption of bone to increase serum free Ca2+. I understand also that you get hemosiderosis, which is why the tumor becomes brown. No clue why you get hemosiderosis though... I know that hemosiderosis is a key characteristic of hemochromatosis, and occurs because the body is overloaded with iron which cannot get out -> macrophages eat up the iron.

Is it possible that the brown tumors hemorrhage and macrophages gobble up the iron, leading to hemosiderosis?
 
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pathologyDO said:
My understanding is that the brown tumors form as a result of primary hyperparathyroidism, where the osteoblasts are working overtime to increase resorption of bone to increase serum free Ca2+. I understand also that you get hemosiderosis, which is why the tumor becomes brown. No clue why you get hemosiderosis though... I know that hemosiderosis is a key characteristic of hemochromatosis, and occurs because the body is overloaded with iron which cannot get out -> macrophages eat up the iron.

Is it possible that the brown tumors hemorrhage and macrophages gobble up the iron, leading to hemosiderosis?
Click to expand...

What happens with rapid tissue breakdown and remodeling?
 
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really a nice thread.
let me ask a Question.
how will we differentiate the following 3 diseases.
1. MGUS
2. Multiple myeloma
3. waldenstrom macroglobulinemia

all of them are plasma cell dyscrasias
 
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with metyrapone stimulatinon test in adrenal insufficeincy, it says acth remains decreased, thats an error right? its on the proposed errata but didnt make it to the official errata. I think acth would be increased, and cortisol would remain decreased
 
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a 35 African American women presents with dyypnea. she has violaceous rash on nose and cheeks she also complains of blurry vision. on Xray chest large hilar L nodes are detected. labs showed a calcium level of 12mg/dl.
mechanism of this hypercalcemia is?
a. increased GI absorption of Ca
b. bone resorption
c. renal retention
d. incresed PTH
e.
 
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a 35 African American women presents with dyypnea. she has violaceous rash on nose and cheeks she also complains of blurry vision. on Xray chest large hilar L nodes are detected. labs showed a calcium level of 12mg/dl.
mechanism of this hypercalcemia is?
a. increased GI absorption of Ca
b. bone resorption
c. renal retention
d. incresed PTH
e.
 
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I got an interesting question from a COMSAE where they asked about what the first sign/symptom a T1DM patient taking insulin and getting ready to go into hypoglycemia would experience so that they know when to get some glucose in them? Ideas?
 
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well hypoglycemia- cortisol, epi, and glucagon would get stimulated. so probably sympathetic respopnse symptoms, ie sweating tachycardia palpiations etc. tahts why apparently B blockers "mask" hypoglycemia or whatever
 
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Ah yes that's what it was! He was also taking a beta blocker - so they wanted to know which symptom would be noticed while taking a beta blocker
 
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hmm.. so all Beta effects are gone, so id assume sweating maybe, even though sweating is a sympathetic response it has cholinergic receptors, so beta blockers couldnt stop that? idk, good question though.
 
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Dr.serotonin said:
a 35 African American women presents with dyypnea. she has violaceous rash on nose and cheeks she also complains of blurry vision. on Xray chest large hilar L nodes are detected. labs showed a calcium level of 12mg/dl.
mechanism of this hypercalcemia is?
a. increased GI absorption of Ca
b. bone resorption
c. renal retention
d. incresed PTH
e.
Click to expand...
I'm quite sure it is A. I don't remember the exact "molecular" reason but in the sarcoidosis there is a over production of vit D by granulomas cells leading to an increased Gi absorption of Ca.
 
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Gdl88 said:
I'm quite sure it is A. I don't remember the exact "molecular" reason but in the sarcoidosis there is a over production of vit D by granulomas cells leading to an increased Gi absorption of Ca.
Click to expand...

correct. the granuloma cells synthesis 1 alpha hydroxylase. increasing Vit D synthesis.
 
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Immigrant from Africa who has been in US for > 9 months.
Which Nematode is the most likely to be the cause of eosinophilia?

a. Pinworm
b. Strongyloides
c. Hookworm
d. Trichuris
e. Ascaris
 
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pinworms dont invade i believe, so that narrows it down i guess. I think judging by th ename ill pick hookworm(old world worm or something)
that or ascaris.
 
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Congrats to everyone on their scores! hoping to get 240+. Do the dipine ca+ channel blockers casue reflex tachy? obv the non-dipines dont as they cause av block..but dont know about the vessel selective ones. Also w/the use of nitrates, the chart in FA says the ejection time is decreased, is thi bc of the reflex tachy?
 
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Coming back to this thread after getting my score back I wanted to say that it got me at least 1 point correct on the real deal (thanks @Transposony ) which can not be found in UFAP (and most of the other sources).
 
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Transposony said:
Immigrant from Africa who has been in US for > 9 months.
Which Nematode is the most likely to be the cause of eosinophilia?

a. Pinworm
b. Strongyloides
c. Hookworm
d. Trichuris
e. Ascaris
Click to expand...

This thread is so much fun!

I would go with Ascaris lumbricoides, as a classic eosinophilic presentation.

Key point: Both ascaris lumbricoides and hookworm invade. The invasion is from the larval stadium. Ascaris invades from small intestine. Hookworm invades through skin. Both can reach the Lung.

Ascaris lumbricoides
found in warm, tropical climates and common in children.

... → worms in small intestine of infected → eggs in stool → fecal-oral transmission → eggs in small intestine → larvae: penetrate small intestinal wall → invasion → can migrate to lungs → ...

Presentation: GI symptoms; Pulmonary symptoms (loeffler's syndrome: eosinophilic pneumonitis, when worms in lungs)

Diagnosis: Eggs on stool, Eosinophilia

Treatment: Albendazol

Other answers:
Pinworm: MC helminth infection in the USA. Look for perianal itching, Dg with famous "scotch tape test". Treat with Albendazole.
Hookworm: ... worms live in small intestine * → eggs in stool → eggs become larvae outside of the body → larvae penetrate skin → go into pulmonary system → swallowed → mature to worms in small intestine → ...
Presentation: Anemia + malnutrition. * (attach to mucosa → malnutrition; bleeding)
 
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aspiringmd1015 said:
can someone elaborate on the difference b/w reaction formation and suppression
Click to expand...

Hi

You're talking about "defense mechanisms" here, that are subdivided in: immature and mature.

Reaction formation is an immature defense mechanism. Think about a woman who wants to get a divorce and behaves overly generous and kind toward her husband. So.. impulses and feelings are transformed into its opposite.

Suppression is a mature defense mechanism. Unwanted feelings are being suppressed in order to cope with reality. Think about a man who is in love with someone but constantly says that he doesn't like the person at all.

[1] http://www.utahpsych.org/defensemechanisms.htm
 
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aspiringmd1015 said:
Congrats to everyone on their scores! hoping to get 240+. Do the dipine ca+ channel blockers casue reflex tachy? obv the non-dipines dont as they cause av block..but dont know about the vessel selective ones. Also w/the use of nitrates, the chart in FA says the ejection time is decreased, is thi bc of the reflex tachy?
Click to expand...
Non Dipine Ca channel blockers depress both the vascular tone and SA/AV node activity,so they don't cause reflex tachycardia. The dipine ones instead act only on vascular tone so that they cause an increase of heart frequency.

The effect of nitrates on Ejection time I think depends on the reduction of preload. A reduction of the preload causes a decrease in contractility ( frank starling law) and so a longer ET....I'm not sure.
 
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Non Dipine Ca channel blockers depress both the vascular tone and SA/AV node activity,so they don't cause reflex tachycardia. The dipine ones instead act only on vascular tone leading to an increase of heart frequency.

The effect of nitrates on Ejection time I think depends on the reduction of preload. A reduction of the preload causes a decrease in contractility ( frank starling law) and so a longer ET....I'm not sure.
 
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Keto said:
This thread is so much fun!

I would go with Ascaris lumbricoides, as a classic eosinophilic presentation.

Key point: Both ascaris lumbricoides and hookworm invade. The invasion is from the larval stadium. Ascaris invades from small intestine. Hookworm invades through skin. Both can reach the Lung.

Ascaris lumbricoides
found in warm, tropical climates and common in children.

... → worms in small intestine of infected → eggs in stool → fecal-oral transmission → eggs in small intestine → larvae: penetrate small intestinal wall → invasion → can migrate to lungs → ...

Presentation: GI symptoms; Pulmonary symptoms (loeffler's syndrome: eosinophilic pneumonitis, when worms in lungs)

Diagnosis: Eggs on stool, Eosinophilia

Treatment: Albendazol

Other answers:
Pinworm: MC helminth infection in the USA. Look for perianal itching, Dg with famous "scotch tape test". Treat with Albendazole.
Hookworm: ... worms live in small intestine * → eggs in stool → eggs become larvae outside of the body → larvae penetrate skin → go into pulmonary system → swallowed → mature to worms in small intestine → ...
Presentation: Anemia + malnutrition. * (attach to mucosa → malnutrition; bleeding)
Click to expand...

Larval stages or Strongyloides
 
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