How to Prepare for the USMLE: Learning from Mistakes

January 26, 2007

I have always insisted on making my own mistakes. I often have to repeat my mistakes. This eats up a lot of my time.

I’ve griped before about not knowing how to handle this period of studying for the USMLE. What I have really meant is that I don’t trust anyone else’s advice and insist on screwing up a little before getting it right.

“You’ve bought too many books, you’ll never read all of those.”
“I never did a single question and got a 99.”
“Just stick with First Aid. It’s all you need.”
“You don’t have to study Emrbyo. There were hardly any Embryo questions on the test.”
“Do nothing but questions. Questions, questions, questions.”
“Man! There were a lot of Emrbyo questions! It’s definitely high yield.”

I still believe now what I believed before: that I have one shot at this test (I have no intention of failing it). In statistical parlance, this means that n=1 and df=0. You cannot draw conclusions from that study. People peddling specific advice to you forget this. Both people that stopped me in the library with their two cents about Emrbyo forgot this. And I will slowly forget this.

Since I broke up the subjects into General and Systems (the organization of the 2007 First Aid), I’ve tried to work on each section a little differently to see what is working. So after Biostats, Behavioral, Embryo, Biochem, Immuno, Autonomic Pharm, Basic Path and Micro, n=8. What follows is a breif chronical of my personal mistakes.

Biostatistics – 1 day

I read through the First Aid section briefly before slowly going through my old notes. I then opened up the Kaplan Lecture notes and read their Biostats section. For the first time, I started to notice that there were disagreements between sources. This sort of thing drives me mad, so I would often waste ten minutes on a piece of minutia to protect the house of cards. I then read the HY Biostatistics by Glaser. It was, by far, the best thing out there. I can’t say enough nice things about this excellent book. Finally, I took out a few pieces of paper and wrote a few pages of notes that I will later use to refresh the week before the test. I spent too much time on this section. I should have just used HY Biostats and taken my notes straight from it. Could have saved half a day.

Behavioral Science – 2 days

Going in, I am less than enthusiastic. Behavioral Science has always felt a little soft and doesn’t lend itself to learning a few core principles and then extrapolating the rest. It’s low yield. I start with Kaplan. It’s overkill. All of the epidemiology is over the top and I am falling asleep. Many of the tables and charts start to conflict with each other (two sentences each claiming different #1 killers for this or that) and I pitch it. After taking a look at the First Aid, I’m desperate to believe that there isn’t much I need to know as I finally turn to the HY Behavioral by Fadem. Everything is compact, well explained, and of a manageable size. This is what I wanted from the beginning. I take all of my notes for later review from this book and move on.

Embryology – 2 days

I wanted to work on Embryo as its own topic, and in the Kaplan notes it is intertwined with each system under Anatomy. Trying to learn from the previous three days, I head straight for the HY Embryo by Dudek (the BRS is also written by Dudek). This book is long, filled with pictures, and weighs in at 177 pages. I really liked this book for its clear explanations. There were several shaky concepts that were finally made clear (meiosis v mitosis, I’m embarassed to say) and it was worth the investment. It was detail heavy, but not to the point of being irrelevant and included plenty of pages devoted to genetic disease. All of this ended up tying in neatly with Biochem, so I consider it time well spent. Two days is a lot to devote to this, but I figured it was worth it on the assumption that it would help me make more connections down the road. I took all my notes onto Post-Its and put them in the First Aid section. I would do this the same way again.

Cell and Molecular Bio – 2 days

At SGU, genetics was a sort of half-assed course. Unfortunate, because I love this stuff and was completely put off at the time. I tried to repeat the success of Embryo with the HY Cell and Molecular Biology book by Dudek.

What trash.

This book has a bizarre number of typographical, illustrative, and conceptual errors. To be sure, there were some bright spots. The first chapter on cell signaling is fantastic and chapter 10: The Human Nuclear Genome was just fascinating, but I spent so much time trying to fact-check this book (after you find one error, you find another, and another) that I reached the point where I just couldn’t trust it any more. It’s largely cobbled together from his other books (almost twenty pages are straight from his HY Embryo) and the patchwork shows. This book was far from high yield and cost me two days before I gave up. I would never recommend it. I decide to cut my losses (Chapter 17 of 27) and go to the next topic.

Biochemistry – 5 days

I spent the first two days doing nothing but looking at the First Aid and reading through the corresponding notes from my first year. At the time, we were using Lipincott’s Illustrated Biochemistry, so having the book next to me made it easy to make sense of my chicken-scratch. I was cruising through the topic, confident, and then an amazing thing happened: I realized how much I didn’t know. You forget about it at the time, but going through Lipincott in first year, every term is alien, every disease and drug tie-in is ignored, and you’re happy to just get a “feel” for what’s going on. The second time around, it’s like seeing the world with new eyes. You understand every reference and all the things that haven’t made sense in other courses are finally connected. It was relevatory. I had originally planned to skim this book but finally decided to reread the whole thing. I didn’t have time to take any formal notes for later review (the Fed-Fast chapters were too engrossing), so I’ll have to carve this out later. This was also the weakest section in the First Aid, and I found myself wasting valuable time fact-checking Lipincott against First Aid against other texts to keep my head on straight.

If I had it to do again, I would have read through my old notes once, and then started on the book. I would have then used the two days that I wasted on Dudek’s HY Cell and Micro to write some review sheets. Oh well. My roommate spent the entire period going through Kaplan’s notes and had positive things to say. I wish I could confirm, but I ran out of time.

Immunology – 2 days

This was another SGU course that fell short for me. Fortunately, you can’t escape it, so that I didn’t learn it formally didn’t stop me from picking it up in Micro, Path, Pathophys, and Pharmacology of Immunosuppression. To get a feel for the scope, I cruised through First Aid and found that I had already covered a great deal of the material in Dudek’s HY Embryo. At this point, I’ve stopped looking at Kaplan all together. I went through the first four chapters of Rapid Review: Immunology and Microbiology. It is bare bones. They make it very obvious what they think is important and I did manage to make some new connections in these chapters, but it was not good enough to be a stand alone. There were several things (like lymph tissue anatomy) that were covered more in depth in the First Aid. I didn’t think that was possible, but there you have it. Between the two of them, I was reintroduced to everything that I saw in Path and my bases are covered. I even had time to take some good review notes for later. For the material I covered, I spent too much time in this book. That said, I didn’t have the time to read a proper text, so, c’est la vie.

Pathology of Neoplasia and Inflammation – 1 day

Path, how I’ve missed you. I’ve been looking forward to cracking open my brand new beautiful Path BRS since the day I bought it, and it was hard to limit myself to these two sections. I like the layout of the book, that the pages are thick enough that highlighter doesn’t bleed through (a previous problem), and the pace. The questions at the end of each chapter are inappropriately easy, which disappoints me. The subject came as a welcome break and I took one page of notes from the BRS and the First Aid.

Pharmacodynamics, kinetics, and ANS – 3 days

I started by reading the sparse entry in the First Aid on dynamics and kinetics before opening my Pharmacology for the Boards and Wards book. It covers these topics in the first 12 pages. It took my three hours. I’m probably just dense, but I didn’t feel this was well presented in either place, so if you already understand the topic, then FA might be enough. I floundered in this, but by the end was happy with my understanding. That left two days to cover autonomic pharmacology. That might have been enough, but the pace to date was too exhausting, and my roommate and I decided to quit for a day and recharge. It was necessary and we felt like a million bucks, but this means that I haven’t covered adrenergic drugs yet and will have to make it up later. If I had this to do over again, I would have traveled back in time and learned it correctly the first time. I also wouldn’t have tried to plow through three weeks of work without a single day off. Live and Learn.

I took a look at the Kaplan pharm section, and they have some very interesting pictures and graphs for conveying difficult topics. There pictures on the effects of cholinergics and adrenergics on the heart rate and BP are amazing, and the picture showing the ionization of drugs in the urine at varying pHs and resulting excretion is one of the most amazing pictures I have ever seen. As Pharm for the Boards and Wards is frustratingly filled with errors, I think I’ll switch over to Kaplan’s pharm when it comes to the systems.

Microbiology – 8 days

This is our first big topic, one of our weakest topics (competing with Pharm), and something I was afraid to begin. I decided to take a completely different approach and this has been the most successful to date.

I read the basic information in my main text, the RR: Immuno and Micro. Although it was painful to admit, I had to relearn about gram negative, positive, and the differences therein. After making some very basic notes, I used the FA bacteria-trees for gram positive and gram negative bacteria. I then wrote out all of the toxins for each bug and came up with some mnemonics for them. This would be my base. I spent the rest of the day writing the best notes that I could, trying to combine all the relevant information from the FA and the RR so that I would never have to look at either again. This took all day.

The next day I spent the first two hours trying to recreate the list of toxins from memory and draw the bacteria trees from memory. I accomplished this by noon. For the next two days, I did nothing but read about antibacterial drugs, their mechanisms, targets, and side effects. Every morning I would reread the notes I had made from the previous day until they were almost second nature. I tweaked my mnemonics.

By the time I had to sit down and learn about each bacteria, I found I knew almost everything I needed to simply from the drugs, the bacteria tree, and their toxins. Everything new that I was reading fell neatly into my pre-existing framework and this made everything before and after more solid for me. All in all, I spent four days on the bacteria alone, two days on viruses, and two days covering the remainder (protozoa, helminths, fungi). Nothing I have done has worked out so well.

Because the pharm section in the RR is small, I had to supplement it with the FA (suprisingly complete) and the Boards and Wards book (this section wasn’t too bad).

General Reference Book

Of all my decisions so far, the best one has been to have the Merck Manual with me at all times. It covers Micro, Pharm dynamics and kinetics, Path, Phys, EVERYTHING. It has been the great oracle whenever my review books conflicted and I would be lost without it. Of course, you could always study with your computer on and the internet running, but that would be a disaster for me. Instead, I keep my focus and have this book in front of me at all times

So what have I learned?

Less is more. Some books should generate automatic refunds for all the mistakes in them, and I would have done much more research on reviews before buying many of them (as it was, I went by First Aid’s recommendations alone). Instead of finding one incredibly solid book for each section, I have at least two books for every section (considering Kaplan) and sometimes three (Pharm, Path). This has been a mistake so far and one I’ll try to avoid as we enter systems.

First Aid is not enough. It has errors and will not give you an understanding of the topics. The First Aid is for someone that already knows everything and is looking for reinforcement and an idea of concepts previously tested. While it may be true that most questions you’ll see have their answers in the FA, that’s a far cry from being able to say that the FA helped me answer all the questions. After you read it, you’ll understand what I mean.

Repetition goes a long way. I find that writing out the information and making my own set of notes has worked for every class I have taken in medical school and this is no different. To paraphrase the late Frank Netter, “you can’t lie in a painting.” I feel the same way about writing: the things that are unclear to you become obvious when you try to take notes. It is, however, incredibly time consuming and I’m 3/4 towards my very own carpel tunnel syndrome. I’ve also found that taking notes on a piece of paper folded down the center is helpful, with prompts on the left and the information hidden on the right. It’s an idea stolen from teh Cornell method of note-taking, and it makes it very hard to lie to yourself as you read something that, “yeah, I remember that.”

When the answer is hidden, there’s no way to fake it.

So if you believe my experience, here’s what you keep and what you throw away from my original list:

  • HY Biostatistics (great)
  • HY Behavioral (great)
  • HY Embryo (for the motivated student)
  • HY Cell and Molecular (trash, don’t buy)
  • Lipincott’s Biochem (long, great if it was your text book. Might want to consider Mark’s BRS)
  • Pathology BRS (great)
  • Pharmacology for the Boards and Wards (look for something better)
  • RR: Immunology and Microbiology (Straight to the point, no frills)
  • Kaplan lecture notes (Biochem and Pharm are strong sections. Biostats and Behavioral are weak. A wash).
  • Merck Manual (my rock)

Hope it helps, topher.

Return to USMLE Step 1 page.


Errors and Problems in High Yield Cell and Molecular Biology

January 13, 2007

These last two days have been exhilirating and frustrating. Exhilirating because I’m exposing myself to incredible concepts in Cell Biology that make me want to live in a lab for the rest of my life to discover more; frustrating because of the vessel. Dr. Dudek’s High Yield Cell and Molecular Biology (2nd Ed. 2007) is riddled with errors in grammar, spelling, punctuation, etc. As an English marm, I find this incredibly distracting. Further, there are a number of times where the book is not internally consitent (i.e. page 10 contradicts page 20), presents concepts in obfuscating ways (this may just be me being dense), or makes factual errors.

I didn’t schedule the time to spend a few hours each day trying to decipher conflicting statements. Though I found sections of this book amazing, the confusing tradeoffs weren’t worth it. If I were to do it all over again, I would not buy this book.

But if you did buy this book and just searched for “errors in High Yield….” then what follows is what I’ve found. This comes from an email I composed to Dr. Dudek, notifying him of the problems. You have to appreciate an author that gives out their email address like that.

Comments are arranged by Chapter-Page-Section. Important errors are underlined and emboldened. Please escuse my hubris:

Chapters 1-13 (out of 26)

  1. The Cell Membrane
    1. P.6, A.13.17: Abbreviation “DST of the loop of Henle” not explained. I knew this term as Thick Assending Limb and not Distal Straight Tubule.
    2. P.7, B: “across the membrane and [verb?] generally called ion channels.”
    3. P.10, B.2: Title: “Transmitted-gated ion channels” should be “TransmitteR-gated…”
    4. P.11, B.2.c: “..the gate is opened and the influx and Na+ and efflux..” “And” should be replaced with “of”.
    5. P.11, B.2.d: “Purinergic 2x” conflicts with P.16, E: “Purinergic 1,2y” These may be different; I raise it only because both are found on “peripheral terminals of nociceptive neurons.”
    6. P.13 is amazing, by the way.
    7. P.14, C: “..trimer with GDP bound to the [alpha] chain..” The [alpha] should have a “q” after it.
    8. P.15, B: You refer to the actions of both Beta-agonists and Beta-antagonists as having “(positive chronotropism; B1 effect).” This is confusing. As I’ve seen it, these drugs are typically described as being “negatively or positively chronotropic” for antagonists and agonists, respectively.
    9. P.16, C: You have the PLc pathway as producing a “[down arrow/decrease in] IP3 + DAG” when it actually produces an increase in IP3 and DAG.
    10. P.18, P.4: last sentence: “…receptor antagonists and are used to [verb?] opioid toxicity…”
    11. P.21, VII: last sentence: “When LDL … binds to the LDL receptor, receptor-mediated endocytosis [verb?] in the following steps:”
    12. P.21, VII.C: You abbreviation “HNG-CoA reductase” should be “HMG-CoA reductase.”
  2. Cytoplasm and Organelles
    1. P.23, I.E: “…and a DNA-binding region that activate gene…” It should be “activates.”
    2. P.30, C.2: last sentence: “The absence of glucose-6-phosphatase enzyme in skeletal muscle prevents the degradation of glycogen to free glucose,” while certainly correct, is confusing if you don’t already know that this absence is normal, and that no skeletal muscle has this enzyme. Without this context, I would have read this as being a disease state. I think it could be reworded:
      1. “Skeletal muscle lacks glucose-6-phosphatase, thereby committing the stored glycogen to be used by the muscle in glycolysis.”
    3. P.32, Figure 2-2, O: “High magnification of a mitochondria with tubular cristae.” The significance of mitochondrial tubular cristae in steroid-secreting cells was not addressed in this chapter.
  3. Nucleus
    1. Figure 3-2 was really helpful
  4. Protein Synthesis
    1. P.38, II.A: “DNA sequences that flank the gene sequence at the 5′ end of the template strand are called upstream sequences. DNA sequences that flank the gene sequence at the 3′ end of the template strand are called downstream sequences.” This is not correct and conflicts with every mention to follow of upstream/downstream sequences, i.e. P. 95-97.
      1. Template strand: upstream: 3′ of gene
      2. Template strand: downstream: 5′ of gene
      3. Non-template strand: upstream: 5′ of gene
      4. Non-template strand: downstream: 3′ of gene
    2. P.43, Figure 4-3: For some reason the last drawn ribosome has the two subunits separated.
    3. P.44, Figure 4-4, A(3): After giving the translation of each codon-to-amino acid sequence, you omit that UAA codes for STOP. I think that this should be included for completeness.
  5. Chromosomal DNA
    1. P.45, II.B: “…impart a positive charge to the proteins that enhances it binding to…” It should be “..enhances its binding to…”
    2. P.46, II.C: “(an enzyme can pass on DNA double..” This should be “can pass one DNA double”
    3. P.46, II.D: “During metaphase of mitosis, [subject?] can become…”
    4. P.46, III: last sentence: “Microtubules produced the by centrosome…” should be “by the centrosome“.
  6. Numerical Chromosomal Abnormalities
    1. P.54, II.B: You state that chimerism is the “reverse of twinning.” While I understand what you are going for by way of analogy, genetically-speaking, chimerism is not the reverse of twinning and this analogy is potentially confusing.
    2. P. 57, Figure 6-3, (A,B): When describing Patau syndrome, you list “fingers flexed and overlapping” as a key feature. This is a key feature of Edwards syndrome.
    3. P.61, III.I. The notation for each of the multiple myeloma translocations is out of order, i.e. t(14;4), t(14;6), t(14;11) should instead be t(4;14), t(6;14), t(11;14).
    4. P.66, VII.A: last sentence: “…encodes for DNA polymerase eta[?] that is involved…”
    5. P.66, VII.C: missing comma between “hypogonadism” and “microcephaly”
  7. Structural Chromosomal Abnormalities
  8. Chromosome Replications and DNA Synthesis
  9. Meiosis and Genetic Recombination
    1. P.82, Figure 9-2, A: This figure is confusing because the end product shows only a swapped intermediate sequence and does not show how the remainder of the chromosome arms can be switched between the two chromosomes using a Holliday junction. This site has a very good demonstration that might be adapted to fit the space of this page.
  10. The Human Nuclear Genome
    1. P.87, III.F-H: These descriptions are great, but why is there no reference to Figure 12-3 (P.104) which shows how each of these works? Most of the information here is also repeated word-for-word in chapter 12. I think moving Figure 12-3 into this chapter and then (instead of repeating the information) simply referencing III.F-H when the time comes in chapter 12 would help.
    2. P.89, V.C: “Simple variable number tandem repeats (VNTR) polymorphisms called microsatellite DNA or SSR polymorphisms … are typically found in microsatellite DNA.” This is self-referencing and confusing. I don’t know what you mean when you say that microsatellite DNA is typically found in microsatellite DNA.
    3. P.91, Figure 10-2 (F): It was my understanding that two transposons, flanking a gene, carrying out gene transfer required the “cuts” to be on the outermost edges of the transposons, thereby incorporating both transposons with the gene into the new location. This figure shows the gene being transferred without accompanying transposons.
  11. The Human Mitochondrial Genome
  12. Control of Gene Expression
    1. P.07, II.B.3: “CREB (cAMP response element binding protein) binds to the CRE in response to elevated cAMP levels in the cell caused by a protein hormone binding to a G protein-linked receptor and thereby induces gene expression.” I found this sentence very confusing. Because the sequence of events is very linear, I think a more linear sentence is appropriate:
      1. “A cell signal produced by a G protein-linked receptor (resulting in an increase in cAMP) triggers CREB (cAMP response element binding protein) to bind to CRE.
    2. P.100, Figure 12-2 (A): The drawing of the folded Homeodomain protein has the COOH terminus and NH2 terminus switched.
    3. P.101, V.D: “There a[are?] several human genes that [verb?] two or more alternative promoters which…”
    4. P.101, V.D: “Alternative promoters start transcription from different versions; the first exon, which is then spliced into a common set of downstream exons, which produce an isoform of the same molecular weight.” This should say:
      1. “Alternative promoters start transcription from different versions of the first exon, which is then spliced into a common set of downstream exons, and produce isoforms of the same molecular weight.”
    5. P.101,V.D: “…but different amino acid sequences in the NH2-terminal end.” This should say “…but different amino acid sequences in the COOH-terminus.”
    6. P.102, V.G: “…~20% of the total genes on the X chromosome escape inactivation. These ~20% inactivated genes include…” This is contradictory. This should say “These remaining active genes include…”
    7. P.103, VI.D.4: “Glucose and lactose(+)” should be “Glucose(-) and lactose(+).”
    8. P.104, Figure 12-3 (D): “Note that each alternative promoter uses in own first exon” should be “promoter uses its own.” “The size of the dystrophin isoforms are show” should be “shown.”
  13. Mutations of the DNA Sequence
    1. P.107 III: You describe nonsense mutations as producing “non-functional (truncated) proteins” and frameshift (or DNA splicing) mutations as producing “non-functional (“garbled”) proteins.” According to the mechanisms described, both frameshift and DNA splicing mutations can produce “garbled” and truncated proteins.
    2. P.107-108, III.F-G: After stating that Translocational and Unstable Expanding Repeat Mutations have been previously covered (and you reference them), you reprint the text. I think you could save this space.
    3. P.109, IV.A: No examples given of haploinsufficiency but several examples given for gain of function mutations. I would have liked to read about a few of them.
    4. P.110, IV.B: “In order for gain of function mutations to become clinically relevant, the individual needs to be heterozygous (i.e. Rr).” Because homozygotes are not excluded (through inheriting these traits), I think it is more correct to say that:
      1. In order for gain of function mutations to become clinically relevant, the individual needs to have at least one copy of the gene (i.e. Rr or rr).
    5. P.110, IV.B.1: “Pittsburgh variant is a missense mutation in the [alpha]1-antitrypsin protein that produces a gain of function mutation known as the Pittsburgh variant.” This is confusing. I do not know what you mean to say that Pittsburgh variant produces Pittsburgh variant. “…methionine358 in the reactive center acts a bait for…” should be “…acts as bait…”
    6. P.110, V: “Fourth, a polymorphism is the occurrence of two or more alleles at a specific locus in a frequencies greater than can be explained by mutations alone (a polymorphism does not cause a genetic disease).” I found this explanation confusing and it does not mention that it is judged on the characteristics of the population that carries it. I think that the Oxford definition is less confusing:
      1. The occurrence of two or more alleles for a given locus in a population where at least two alleles appear with frequencies of more than 1%.
    7. P.110, V.A.2: When writing about Unequal Sister Chromatid Exchange, you write that: “…cleavage and rejoining of sister chromatids occurs at different positions on the maternal chromosome usually within a region of tandem repeats.” followed by the exact same sentence, changing only “maternal” to “paternal.” I think you should change this into one sentence, reading:
      1. …cleavage and rejoining of sister chromatids occurs at different positions on the (maternal/fraternal) chromosome usually within a region of tandem repeats.”
    8. P.111, V.A.3: When describing replication slippage, you don’t mention that the strand that is slipping either “forward” or “backwards” refers to the parent or daughter strand (respectively). You also don’t mention that the insertions and deletions only affect one arm of the sister chromatid. I think you should expand the description of replication slippage and include something similar to this figure (click to enlarge) that illustrates that the templates are unchanged, therefore there is a 50/50 chance that no insertion or deletion will be passed on.
    9. P.114, Figure 13-1 (G): “PNA splicing” should be “RNA splicing”

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