62 of 63 people found the following review helpful:
5.0 out of 5 stars
How to ace the USMLE Step 1: what you REALLY need to know (from a guy who broke 260 without killing himself studying), July 30, 2005
I actually used the 2004 edition of First Aid, but it doesn't change much from year to year. Here is what you need to know about how to ace the USMLE Step 1:
1. First Aid is your bible. Read it, study it, know it. I honestly believe that if you had this book memorized cover to cover and nothing else, you would do very well on the USMLE Step 1.
2. Use Kaplan QBank. I recommend completing most of it (the regular QBank, not the IV QBank, which I didn't use), but you don't have to finish all of it. Keep a list of your errors and review your list periodically (at least twice per week) before you do more questions.
3. The BRS books are useful for fleshing out your review of physio and path. Use them during your courses if possible.
4. "Clinical Microbiology Made Ridiculously Simple" has great pictures to help you remember micro stuff. It's best if you use it during your micro course, then just skim the stuff you highlighted to help you solidify micro before the boards.
5. First Aid is pretty spotty on anatomy (which includes embryology, gross anatomy and neuroanatomy) but there really is very little anatomy on the USMLE Step 1. It's a subject you can get very bogged down in with pretty low yield (as in a whole book on neuro, embryo and gross for a few questions on the actual exam, and will you even remember the details anyway?), and you won't lose many points by just using First Aid for this subject. I actually ended up reading High Yield Gross, High Yield Embryo, and Clinical Neuro Made Ridiculously Simple, and I think it was mostly a waste of time because of how little I retained. Clinical Neuro Made Ridiculously Simple isn't a bad book to have in general, though--it cleared up a number of clinical points not well-covered in my neuro course.
6. For biochem, behavioral science and pharmacology, First Aid is all you need. I know that may sound blasphemous, but trust me. It's what I did and look at my score. There may be one or two questions that come up during the exam on things you've never heard of, but it's not worth all the extra time you'd put into going through other whole books or overly comprehensive sets of flashcards. And would you remember the obscure things anyway?
So that's all you need. Remember, when it comes to test day it's not what you went over that counts but what you REMEMBER. Repetition with First Aid (and BRS physio and path) will help you more than grazing over several review sources on each subject. Don't waste too much time on anatomy. And if you study like I did, you can still have a life (sort of) while studying for the boards! GOOD LUCK!
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17 of 17 people found the following review helpful:
2.0 out of 5 stars
Errata, December 20, 2006
This review is from: First Aid for the USMLE Step 1: 2006 (Paperback)
I found this in a forum, I won't say anything just read this before you exam:
A bunch of emails have been going around my class with the First Aid 2006 errata..there are tons, and even missing pages!!!
I've copied & pasted what I can find so far, and obviously, use at your own risk but most are obvious... and 2 attachments of 2 PDF files of missing pages - one for micro (Rickettsia) & Cardio drugs.,
age#--correction
72--it should read "Kubler-Ross Dying Stages" (not grief stages)
161--Micro - Most common cause of bacterial meningitis in adults 18-60 is Strep pneumo. N meningitidis is still the most common for 6 - 18 yr olds (from uptodate)
187--the complement cascade show C4b2*b* as classic C3 convertase and C4b2*b as classic C5 convertase. It should be C4b2_*a*_ = classic C3 convertase and C4b2_*a*_3b = classic C5 convertase
208--St. John's Wort is an inducer of CYP (3A4), not an inhibitor. (checked JAMA)
221--EDV and ESV are swapped in the pressure-volume relationship in the cardiovascular section
221--the PV-curve shows what happens with an increase in afterload AND contractility. So put a little "[up-arrow] contractility" next to "[up-arrow] afterload"
259--In "Other hypothalamic/pituitary drugs" GH is somatoTROPIN. Octreotide is the analogue of somatostatin.
274--Barrett's esophagus is replacement of nonkeratinized squamous epithelium with INTESTINAL columnar epithelium in the distal esophagus (not gastric)
275--"Usually squamous cell carcinoma" Actually, squamous cell CA and adenocarcinoma of the esophagus currently have almost equal incidence due to a rapid rise in adenocarcinoma rates in recent decades (from UpToDate, Qbank)
283--Pirenzepine causes TACHYcardia, not bradycardia as a toxicity (from micromedex)
295--Wilm's tumor is a mutation on 11p (not 11q) (according to BRS and emedicine and Miglet) (for both WT1 and WT2)
310--Imatinib (Gleevec) is NOT an antibody or myclonal. But it is a tyrosine kinase inhibitor.
322--Pemphigus vulgaris = intraEPIDERMAL bullae
344--cavernous sinus syndrome should include opthalmoplegia, opthalmic and MAXILLARY sensory loss
345--swap SR with IO at the top, and IR with SO at the bottom
346--pupillary light reflex sends signal via CN2 not CN3
353--Syringomyelia is from damage to crossing SPINOTHALAMIC TRACT FIBERS in the anterior white commissure.
368--the mechanism of ethosuxamide blocks thalamic Ca+2 channels, NOT thalamic Ca+1
385--#5) SLE - in DIFFUSE PROLIFERATIVE form you get wire-loop abnormality with subendothelial immune complex deposits
Color img 48B--is actually a pilocytic astrocytoma, not a glioblastoma (those are Rosenthal fibers)
Color img 104--Sarcoidosis does NOT have caseation
they're the
area immediately posterior to the central sulcus.
pg 346: Pupillary light reflex -> light in either retina sends a signal
via
CN II (NOT III). the pupils contract bilaterally (consensual reflex)
via CN
III (= solid lines)
pg352- diagram on left: F, which is supposed to be pilocytic
astroctoma, is
usually in the posterior fossa but they drew it in the frontal lobe.
pg353- the spinal cord section diagram for syringomelia- corticospinal
should be spinothalamic
pg 357- herniation syndromes- the uncus is mislabelled.
Differences In the definition of cleft lip on page 117 and 124. What
it
says on page 124 is correct and page 117 should read "failure of fusion
of
the maxillary and medial nasal processes leading to cleft lip."
pg 149 it states that Loa Loa (nematode) is transmitted by the deerfly.
this is incorrect. it is transmitted by the bite of a mango fly,
Chrysops.
Pg 63 - Second chart should be disease vs. exposure, not disease vs. test [Annie Garment]
Pg 87 - Pyruvate Kinase is shown as reversible in the diagram. It's
irreversible. [From Mike Su and Christian Song]
Pg 97 - Liver, Fasting State: Amino acids can indeed enter the TCA cycle directly (after deamination) but this is not true for glycerol or lactate. Glycerol enters the glycolytic pathway by being metabolized to Dihydroxyacetone Phosphate (DHAP) while lactate enters the pathway by being metabolized to pyruvate. Therefore, the arrows should be changed accordingly.
Pg 118 - Under the heading "Embryologic Derivatives", surface ectoderm is said
to give rise to the "epithelial linings". This is mostly incorrect. The ectodermal germ layer gives rise to the *sensory* epithelium of the ear, nose, and eye. Epithelial linings of the gut, UG tract, and respiratory tract are derived from the *endodermal* germ layer. [DT Jacobs]
Pg 140 - "Salmonella has an animal reservoir." Not true of Salmonella Typhi, the strain the causes Typhoid fever! (i.e. it's only in humans).
Pg 141 - E. Coli O157:H7 is a subtype of EHEC, not EIEC.
Pg 154 - The process explained is called "Phenotypic Masking" not "Phenotypic Mixing", which is a different process. I verified this with a research paper which describes the process in the journal of Evolution. [from James Toussaint]
Pg 166 (Chart) - Amoxicillin/Ampicillin can be used for E. Coli, as it says on the very next page.
Pg 302 - Follicular Lymphoma: "bcl-2 is involved in apoptosis." Okay, technically this isn't an actual mistake, but at the very least it's HIGHLY misleading. It should really say "bcl-2 is involved in INHIBITION of apoptosis." It's important to realize that this isn't a matter of underexpression of a pro-apoptotic gene, but rather overexpression of an anti-apoptotic gene.
Pg 319 - Osteomalacia/rickets. Vitamin D deficiency causes a DECREASE in serum phosphate (due to increased renal excretion, which, in turn, is due to increased PTH).
Pg 324 - Temporal Arteritis affects medium and LARGE arteries
Pg 325 - Cox-2 inhibitors: the IMPORTANT toxicity is an increased risk of thrombosis (stroke or MI).
Pg 326 - Etanercept: Mechanism - inhibits BOTH TNF-Ü AND TNF-â
Pg 404, Testicular non-germ cell tumors, Leydig cell: "androgen producing leads to gynecomastia in men, precocious puberty in boys." While it is true that Leydig cell tumors are androgen-secreting (at least initially) and it is also true that later in life
they can lead to gynecomastia, it is incorrect to say that these two facts are
related to each other. Not only does this not make any sense, but it turns out
that adults with leydig cell tumors actually have DECREASED levels of androgens.
Pg 485 - ALL is Acute LymphoBLASTIC Leukemia, not "lymphocytic" leukemia
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