Official Step 1 High Yield Concepts Thread

[Transposony]

---

Members don't see this ad.

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

 

[seminoma]

Hyaline material in the alveoli along with columnar cells. Located peripherally. Imaging shows consolidation. Non-smoker

Diagnosis?

If hyaline material lining the alveolar walls, then probably adenoCIS.

If it's hyaline material in the alveoli (like an exudate) then it could be pulmonary alveolar proteinosis, but less likely bc of the columnar cells.

 

[seminoma]

Corticosteroids have 3 primary mechanisms that help improve asthma symptoms. What are they? (two are inhibitory, one provides synergism with other drugs).

 

[pathologyDO]

If hyaline material lining the alveolar walls, then probably adenoCIS.

If it's hyaline material in the alveoli (like an exudate) then it could be pulmonary alveolar proteinosis, but less likely bc of the columnar cells.

Bronchioloalveolar CA (now called AdenoCIS) was the correct answer!! Hyaline would line the alveolar walls, the cells would be columnar, and this type of cancer is found peripherally

 

[seminoma]

Bronchioalveolar CA was the correct answer. Hyaline would line the alveolar walls so its more like an exudate of sorts, the cells would be columnar, and this type of cancer is found peripherally, similar to adenocarcinoma.

Bronchioloalveolar carcinoma is the old name for adenocarcinoma in situ. The pink lining of the alveolar walls in adenoCIS is just the cytoplasm of the columnar cells, not an exudate as far as I know.

 

[pathologyDO]

Bronchioloalveolar carcinoma is the old name for adenocarcinoma in situ.

Sorry changed my original post. Apparently Pathoma hasn't gotten that change of name memo yet 😉

 

[FutureDO2016]

When can a gender be accurately predicted? I think week 10 via ultrasound?

 

[seminoma]

When can a gender be accurately predicted? I think week 10 via ultrasound?

Did you get a question about this in a qbank? I don't think sex determination is a HY topic...

 

[Transposony]

Cancer cells can't use leucovorin as a substrate in folate synthesis.
I suppose leucovorin could reduce mtx efficacy as an immunosuppressant though.

Leucovorin is folinic acid (activated folic acid).
Methotrexate acts by inhibiting the metabolism of folic acid required for DNA synthesis in both normal and cancer cells.
Leucovorin rescue is used only when Methotrexate causes bone marrow suppression.
Leucovorin rescue is used at the cost of decreasing efficacy of Methotrexate since you are giving what Methotrexate blocks.

 

[dfib slim]

Cheyne-Stokes vs Kussmaul respirations and conditions causing each?

 

[Transposony]

Corticosteroids have 3 primary mechanisms that help improve asthma symptoms. What are they? (two are inhibitory, one provides synergism with other drugs).

 

[FutureDO2016]

My friend vividly told me it was on his exam

 

[seminoma]

Leucovorin is folinic acid (activated folic acid).
Methotrexate acts by inhibiting the metabolism of folic acid required for DNA synthesis in bothe normal and cancer cells.
Leucovorin rescue is used only when Methotrexate causes bone marrow suppression.
Leucovorin rescue is used at the cost of decreasing efficacy of Methotrexate since you are giving what Methotrexate blocks.

When MTX is being used for cancer treatment its efficacy is defined by how well it reduces tumor load. Leucovorin rescue does not reduce antitumor activity. Yes, I should have said cancer cells cannot utilize leucovorin for growth rather than for folate synthesis.

http://www.uptodate.com/contents/therapeutic-use-and-toxicity-of-high-dose-methotrexate

Rationale for leucovorin rescue — As with many other anticancer drugs, MTX has little selectivity for tumor cells, and its effectiveness is limited by toxicity to normal tissue, particularly the gastrointestinal (GI) epithelium and bone marrow. To improve the therapeutic index of MTX, Goldin developed the concept of rescuing normal cells from toxicity by providing reduced folates (leucovorin, also called folinic acid, N5-formyl-tetrahydrofolate, citrovorum factor) to bypass the metabolic block induced by MTX [22]. In these pioneering experiments, administration of leucovorin within 24 to 36 hours after administration of MTX was able to prevent MTX-induced host toxicity without diminishing antitumor activity.

The reason why leucovorin selectively rescues normal but not malignant cells is incompletely understood. The original premise that providing reduced folate would circumvent the metabolic block produced by MTX is not easily explained except in situations where folate transport is deficient in the malignant cells. In such cases, leucovorin cannot be transported into the malignant cell, but it can enter normal cells and compete with MTX for binding sites on DHFR because they retain a normal folate carrier protein [6,23]. If leucovorin is present in sufficient quantities, the enzyme is reactivated, and purine and thymidine synthesis can be reinitiated. This situation is thought to be relatively uncommon.

As noted above, cellular differences in polyglutamation have been suggested as an alternative explanation for selective leucovorin rescue. Intracellularly, leucovorin is able to compete with free but not polyglutamated MTX for binding to DHFR [23]. In contrast to tumor cells, comparatively little PGMTX synthesis occurs in normal gut epithelium and bone marrow precursors under similar conditions [18,24]. It is hypothesized that because of the lower levels of intracellular PGMTX, leucovorin can more effectively curtail DHFR inhibition in normal as compared to malignant cells

 

[faisal 2000]

mechanism of action of clofibrate (and indication ,contraindication)

 

[pathologyDO]

mechanism of action of clofibrate (and indication ,contraindication)

MOA -> this is a fibrate drug that inhibits PPAR-alpha, which is going to increase LPL activity as well as increase HDL levels

Indications -> Hypercholesterolemia, Hypertriglyceridemia

Contraindications -> Used with statins should be avoided because of rhabdomyolysis; hepatic metabolism and increases LFTs, so avoid in live failure

 

[pathologyDO]

What are the 3 risk factors for a newborn developing respiratory distress syndrome?

 

[seminoma]

What are the 3 risk factors for a newborn developing respiratory distress syndrome?

Premature, maternal diabetes, can't think of a third.

 

[faisal 2000]

What are the 3 risk factors for a newborn developing respiratory distress syndrome?

maternal diabetes , c-section,premature infant

 

[pathologyDO]

maternal diabetes , c-section,premature infant

Exactly! Why does c-section cause NRDS?

 

[dfib slim]

Exactly! Why does c-section cause NRDS?

Don't have all that birthing pressure to clear the alveoli or catecholamine release from the stress of it all.

 

[pathologyDO]

Don't have all that birthing pressure to clear the alveoli or catecholamine release from the stress of it all.

Right!!!

And lastly, what would you give a very premature baby delivered via c-section to prophylactically prevent NRDS?

 

[dfib slim]

Right!!!

And lastly, what would you give a very premature baby delivered via c-section to prophylactically prevent NRDS?

Bag down some of that dipalmitoylphosphatidylcholine mixture

 

[pathologyDO]

Bag down some of that dipalmitoylphosphatidylcholine mixture

boom, you got it.

 

[Transposony]

What's the difference between Type II Pneumocytes and Club (Clara) cells as they both secrete surfactant and act as reserve cells to type I cells and other type II cells ?

 

[dfib slim]

Where in the cell does molluscum contagiosum virus replicate?

 

[pathologyDO]

What's the difference between Type II Pneumocytes and Club (Clara) cells as they both secrete surfactant and act as reserve cells to type I cells and other type II cells ?

Would the answer be that Clara cells also detoxify ?

 

[hallowmann]

Would the answer be that Clara cells also detoxify ?

Clara cells are also (edit: non-)ciliated. Also aren't Clara cells mainly in the respiratory bronchioles, not the alveoli? Type II pneumocytes are mainly able to differentiate into Type I's (and divide into more II's). I believe Clara cells have a bit more diversity in their lineages.

 

[pathologyDO]

Alright, not sure whether this would be considered high yield (likely not), but I just got a Kaplan Q similar to this:

Patient is bitten by a cat and develops a fever, along with a tender and swollen lymph node in the popliteal region. Where did the cat bite this patient?

Lateral Dorsum of Foot
Lateral Thigh
Medial Leg, below the knee
Medial Foot Sole
Medial Thigh

 

[seminoma]

Alright, not sure whether this would be considered high yield (likely not), but I just got a Kaplan Q similar to this:

Patient is bitten by a cat and develops a fever, along with a tender and swollen lymph node in the popliteal region. Where did the cat bite this patient?

Lateral Dorsum of Foot
Lateral Thigh
Medial Leg, below the knee
Medial Foot Sole
Medial Thigh

Dorsum of the foot drains to small saphenous vein, which drains to popliteal nodes.
Lateral Thigh - too high to drain to popliteal region
Medial leg, below the knee - drains to great saphenous, which goes to inguinal nodes.
Medial foot sole - great saphenous vein --> inguinal nodes
medial thigh - too high to drain to popliteal

I don't know if lymph drainage is that high yield, but basically lateral leg --> popliteal, medial leg/thigh --> inguinal.

 

[seminoma]

and by "high" I mean "proximal".

 

[pathologyDO]

Who can tell me why patients with chronic autoimmune gastritis get megaloblastic anemia?

 

[seminoma]

Clara cells are also ciliated. Also aren't Clara cells mainly in the respiratory bronchioles, not the alveoli? Type II pneumocytes are mainly able to differentiate into Type I's (and divide into more II's). I believe Clara cells have a bit more diversity in their lineages.

Clara are non ciliated

 

[hallowmann]

Clara are non ciliated

Well, yeah, hence their description of being randomly bald blobs among ciliated columnar epi. That's what I get for trying medicining at midnight 😛.

 

[Transposony]

Well, yeah, hence their description of being randomly bald blobs among ciliated columnar epi. That's what I get for trying medicining at midnight 😛.

Now I am never going to forget Clara cell.

 

[Transposony]

QUESTION. What bacteria would cause osteomyelitis in a sickle cell patient?
UW says it's Staph Aureus, since it's the most causative agent, even in SCD.
However, DIT and Dr. Conrad Fisher both say it's Salmonella in SCD.

Staph aureus is the mc cause even in sickle cell as far as I know. Just like h.flu is the mcc of epiglottitis even in immunized children.

Goljan also says Salmonella MMC with SCD

From UpToDate:

"The most common offending organisms are Salmonella species. Staphylococcus aureus, the most common etiologic agent in patients without sickle cell anemia, accounts for less than 25 percent of cases. Articular infection is less common and is often due to S. pneumoniae."

Here we go again..........UW v/s UpToDate with DIT, Goljan and Fischer sprinkled in between.
I think the winner is Salmonella since even Kaplan (or Becker) also says Salmonella.
FA 2015 says: Salmonella and S. aureus.

 

[faisal 2000]

why reye syndrome leads to hypoglycemia ?

 

[dfib slim]

Vitamin deficiencies leading to hyperhomocysteinemia?

 

[Transposony]

Vitamin deficiencies leading to hyperhomocysteinemia?

Hypocobalaminemia leads to hyperhomocysteinemia leading to homocystinuria.

 

[dfib slim]

Hypocobalaminemia leads to hyperhomocysteinemia leading to homocystinuria.

And the other two?

 

[FutureDO2016]

Patient with history of high blood pressure develops CHF and gets pitting edema in legs, rales in lungs, and tachycardia. Besides a diuretic, what drug do you give him and why...

A)dobutamine B) ace inhibitor C)minoxidil D)nifedipine E) Alpha blocker F)beta blocker

 

[Transposony]

And the other two?

B 6 & 9

 

[CodeRedDew]

Patient with history of high blood pressure develops CHF and gets pitting edema in legs, rales in lungs, and tachycardia. Besides a diuretic, what drug do you give him and why...

A)dobutamine B) ace inhibitor C)minoxidil D)nifedipine E) Alpha blocker F)beta blocker

Ace inhibitor; decrease BP and decreases the cyclic destruction caused by RAAS activation

 

[CodeRedDew]

why reye syndrome leads to hypoglycemia ?

impaired gluconeogenesis?

 

[seminoma]

Here we go again..........UW v/s UpToDate with DIT, Goljan and Fischer sprinkled in between.
I think the winner is Salmonella since even Kaplan (or Becker) also says Salmonella.
FA 2015 says: Salmonella and S. aureus.

Fair enough. I think it's S.aureus unless there is something specifically for Salmonella or against S.aureus. Similar debate as last year or two years ago with the 20 something year old athlete male (N.gon vs S.aur). Some people were saying he was a young athlete so he was probably sexually active (so n.gon). Others were saying there was no indication that he was sexually active (so s.aur).

Indications for salmonella could be obvious ones like culture/gs results, "same secretion system as pseudomonas"; or less obvious things like two answer choices that both apply to s.aureus. For example answer A is "coagulase positive staph" and answer B is "Protein A".

 

[Transposony]

Fair enough. I think it's S.aureus unless there is something specifically for Salmonella or against S.aureus. Similar debate as last year or two years ago with the 20 something year old athlete male (N.gon vs S.aur). Some people were saying he was a young athlete so he was probably sexually active (so n.gon). Others were saying there was no indication that he was sexually active (so s.aur).

Indications for salmonella could be obvious ones like culture/gs results, "same secretion system as pseudomonas"; or less obvious things like two answer choices that both apply to s.aureus. For example answer A is "coagulase positive staph" and answer B is "Protein A".

I'll go with Salmonella if they mention SCD in the question stem.
If no other clue is given, it's Staph aureus.

 

[aspiringmd1015]

anyone know why alcohol/stress causes release of serotonin from carcinoid tumors?

 

[Transposony]

What may be the underlying pathology behind psychogenic polydipsia ?

 

[Transposony]

Which two conditions must be ruled out before making a diagnosis of SIADH ?

 

[Transposony]

Name three cells involved in Type IV hypersensitivity and their mechanism of activation ?

 

[dfib slim]

A toxin antidote that is also used as a street drug?

 

[dfib slim]

Pathogenesis of concentric vs eccentric ventricular hypertrophy?