p53's USMLE Preparation Diary

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p53

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Day 1.
It sure is nice to back from my mini sabbatical. I will post a tell all diary of what subjects I studied for each day until my exam. At the end of each day I will post, some of the things that I reviewed.
Today's goal is to review Behavioral Science. My resources are Rapid Review Behavioral Science and Lange's Behavioral Science in Primary Care.
Don't consider it disrespectful if I don't respond to your post. The purpose of this thread is to give future USMLE testtakers a glimpse/insight of how a student prepares for this beast, not as a pseudo-social or veiled solicitation of sympathy that predominates 90% of the threads in here.
 
p53 said:
Day 1.
It sure is nice to back from my mini sabbatical. I will post a tell all diary of what subjects I studied for each day until my exam. At the end of each day I will post, some of the things that I reviewed.
Today's goal is to review Behavioral Science. My resources are Rapid Review Behavioral Science and Lange's Behavioral Science in Primary Care.
Don't consider it disrespectful if I don't respond to your post. The purpose of this thread is to give future USMLE testtakers a glimpse/insight of how a student prepares for this beast, not as a pseudo-social or veiled solicitation of sympathy that predominates 90% of the threads in here.

How was your five day holiday?
 
HI-YIELD QUESTION OF THE DAY:

p53 sabbatical = Li-Fraumeni Syndrome ?

From the wild blue yonder..
 
USFOptho said:
HI-YIELD QUESTION OF THE DAY:

p53 sabbatical = Li-Fraumeni Syndrome ?

From the wild blue yonder..

Nice. I wonder what a pedigree of Li-Fraumeni Syndrome would look like. If you don't, you better figure it out before you take your $45 NBME exam. I narrowed it down to expressivity vs multifactoral inheritance. The pedigree was easy to figure out, it showed 4 generations of patients with cancer.

Alright, this diary takes a long time. But I'll continue. It will be briefer than I originally planned.
 
5-19 Read through Rapid Review Behavioral Science. I loved the blue boxes in there. The reason I picked Rapid Review was because it was highly rated in First Aid. Plus, the CD for Rapid Review has vignette questions just like NBME. Also, I wasn't impressed with Fadem's figures, and tables. The milestones for a child from birth to 7 is high yield for Step 1 but Dr. Fadem barely discussed it. Big turn off. Also, Dr. Goljan is the main editor for the Behavioral Science book, I figured some of his former students told him some behavioral science content and it influenced the authors. Another interesting thing about the book is that all of the authors are from Oklahoma State. Perhaps the new mecca of medical education is in STILLWATER, OKLAHOME!

The Behaviroal Science in medicine was for the touchy patient-physician conversations and what to say next kind of questions. These things are not discussed that well in BRS or Rapid Review.

Jalby in search engine.
 
5-20 What the Kell did I do Friday? Oh yeah, I started reading the BRS Physiology. The chapters went real slow. I wanted to do all the questions in the book. It took me three days to finish BRS Physiology. I did all of the questions in the book. It was interesting to see how much pharm was in the questions. Which receptor i.e alpha 1, alpha 2, Beta one, Beta two is knocked out with Propranolol. Who would have guessed I would be reviewing Pharm by doing BRS Physio questions? My average was from 100% (Cardio) to 80% (Neuro). Not bad because I haven't really studied neuro yet. Well, I did go through BRS Neuroanatomy in March. One thing I want to make note of is that many people including Goljan believe ventilation is actually best at the Apex of the lung. Actually, ventilation is best at the base of the lung. The reason you get better exchange of gases at the apex is because it has the best Va/Q ratio. Small point, but this is a tricky point and trips many people up. Also, exercise doesn't cause hyperventilation (most people think) rather tachypnea. There is a difference. One last point, Goljan is confusing creatinine with inulin. Creatinine is secreted thus it is an estimate of GFR. Speaking of Dr. Goljan, I am somewhat bothered with the fact that at the end of his first GI lecture, he talks about how the boards have just started testing Robertsonian Translocation in Down's syndrome. Guess what? That exact question was in my pathology shelf exam.

Oral glucose vs IV glucose is high yield. Oral glucose has a higher insulin response (no need to bore with the mechanism). Hmmm...glucagon actually increases insulin release while insulin inhibits glucagon release. Thus, if you have no insulin, the problem is not only clearing glucose but more glucose is made via gluconeogenesis. Interesting. Okay, I digress too much.

One observation I found interesting is that many of my classmates have said, why study for boards in February or over Christmas Break. They argue that you will forget by the boards. This is somewhat true. However, by reading up on things (lightly), it is easier to retrieve it. For example, during Christmas Break I went through BRS Physiology (leisurely read not studied) and I thought I was going to die because I didn't remember jack. Well, now that I'm looking at it again in May, the concepts came back much easier. Same thing with Anatomy, thanks to Jalby's advice I went through Moore's Blue Boxes during Christmas Break. I didn't annote anything just read. Then, I reread the moore blue boxes during spring break. Now, I'm going to reread moore's blueboxes one last time. That is three times through without having to write anything down. Annotating is what takes so long. Don't get me wrong, anatomy will probably still be my weakest subject, however now I will be able to reason out any clincial anatomy questions via logic.

My goal for Step 1 prep is repetition. Today, I'm going through Pharmacology. My strategy is to start with the cancer drugs. This is my second pass through Pharm since early May so it should go by quicker. The drug indications are what intimidates me. Side effects, not bad. Mechanisms, I like them because it is cerebral. If I get a question that asks for the DOC for Tulermia I'm waiving the white flag, it isn't worth knowing.
 
phillyfornia said:
i thought that you were just gonna use goljan audio?

It was a parody to show how silly it is to rely on one source. It requires a strong foundation in basic science to get the most out of goljan's lectures. He is like the ribbon on my Step 1 prep. I still listen to the guy, but he is used to tie concepts rather than learn concepts.
 
One more thing. I know that some of you know friends that have flunked step 1 or had the keen insight to attend one of Dr. Goljan's lectures at Kaplan. If you convince these people to put up their 2005 High Yields on Ebay, you can bet they will easily clear $500 for those notes. If I spent 4 G's for a review course, I would put up the stuff on Ebay to recoup my money. Here is information about Kaplan and Dr. Goljan.

http://www.kaptest.com/repository/t...s/Step_1_Prep/ME_step1_faculty.html#Pathology

If you double click schedule in this link below, you will see the 2005 locations where Dr. Goljan will have his week long pathology lectures with his updated 2005 Lecture Notes and 2005 High Yield Facts (from 2004 USMLE Step 1).

http://www.kaptest.com/repository/t...grams/Lecture_Locations/IMG_step1_dallas.html
 
OSU med school is in Tulsa, not Stillwater.

p53 said:
5-19 Read through Rapid Review Behavioral Science. I loved the blue boxes in there. The reason I picked Rapid Review was because it was highly rated in First Aid. Plus, the CD for Rapid Review has vignette questions just like NBME. Also, I wasn't impressed with Fadem's figures, and tables. The milestones for a child from birth to 7 is high yield for Step 1 but Dr. Fadem barely discussed it. Big turn off. Also, Dr. Goljan is the main editor for the Behavioral Science book, I figured some of his former students told him some behavioral science content and it influenced the authors. Another interesting thing about the book is that all of the authors are from Oklahoma State. Perhaps the new mecca of medical education is in STILLWATER, OKLAHOME!

The Behaviroal Science in medicine was for the touchy patient-physician conversations and what to say next kind of questions. These things are not discussed that well in BRS or Rapid Review.

Jalby in search engine.
 
05-24 The Cancer drugs went smooth. I used Goljan's letter trick often in this section for the side effects. Those that remember, Goljan said that myDriais, D is dilate, miosis is the other one. Same here, vinBlastin is bone toxicity, vinCristine is the other one. Figure 39.1 in the Pharmacology Recall book is golden. Also, tied some concepts today. Doxorubcin and Daunorubicin causes cardiac toxicity. I found out these cause congestive heart failure aka dilated cardiomyopathy. So this made me think about other causes of dilated cardiomyopathy (cocaine, alcohol, "wet" beri beri via Thiamine deficiency (decreased ATP). Then, thiamine made me think about wernieckes and korsakoff (from his audio in the ER you must put up a thiamine bag with glucose). It is easy to get side tracked when knowledge is connected in series. There is the other half that Goljan talks about that Boards people tests you on. "Half way there, blah, blah".

That brings up another trick mentioned by Goljan. He said, he ties things together by lumping them together. He is right it makes things easier. I'll give you another example. While I was reading about the toxic effects of vincristine (peripheral neuropathy), I thought about diabetes. This also causes peripheral neuropathy. So then I got side tracked by thinking about nonenzymatic glycosylation of peripheral myelin. Conversely, if I think about diabetic peripheral neuropathy, I'll think about vincristine also causes peripheral neuropathy. This ties these two things into one memory nugget, rather than two. No wonder Goljan goes off on tangent so much in his lectures, that is how he has stored information. I like that trick. Hmmm, dry beriberi also cause peripheral neuropathy too. That is also caused by decrease in thiamine. Nice little symmetry there.

One thing I want to make note of is Immunopharmacology. I might be going a little overboard on this but I think this is high yield. Therefore, I am not going to cut corners in this section. Yep, that means I am going to read the immunopathology section in Big Katzung. Also, read the 2 or 3 pages of derm pharm in Big Katzung. Everything else should be covered in Pharm Recall or Trevor from Arkansas.

Lastly, after Cancer drugs I started at the beginning. Pharcokinetics and Pharmacodynamics. I didn't have the Goodman book in front of me but I took some notes in that book last time. I want to look at the graphs in those two chapters one more time before I take the test. ONCE AGAIN, THE REST OF THE BOOK IS CRAP FOR STEP 1. Also, I went through Autonomic Nervous System. This section is very straight forward if you know the physiology. Memorizng Dumbelss seems very silly when you can reason out the side effects (just keep in mind skin and sweat glands are sympathtetically dominated). The Blind as a Bat mnemonic is silly too. Then, I reached my chief nemesis in Pharmacology, Central Nervous System. This is my achille's heel in pharm. I fell asleep twice trying to review this section. I realized just reading Kaplan Pharm and Pharm Recall put me to sleep. So I decided to use a different approach, I integrated the stuff with Neuroanatomy by looking at pictures. I am a visual person so this helped big time. I looked over CTs http://www.med.harvard.edu/AANLIB/cases/caseM/case.html and Cross Sections http://medlib.med.utah.edu/WebPath/CNSHTML/CNSIDX.html. This helped out alot. I reviewed the diseases of the basal ganglia, "C"audate Nucleus = "C"horea, Subthalamic Nuclei, substantia nigra (dopamine disinhibition pathway to GABAnergic neurons, aka 2 negatives make a positive pathway) , tubuleoinfundibular pathway (dopamine inhibits prolactin release via D2 receptor). The signal pathway is via cAMP. D2 decreases cAMP, which makes sense since dopamine is an inhibitor in CNS, D1 increases cAMP which makes sense since in the PNS it is an activator (i.e renal vasculature).

That's it. Today, finish up Pharm and work through Pharm questions.
 
I'm confused. Did you take 5/21, 5/22, and 5/23 off? By the way, this is actually pretty interesting but you're going about it the wrong way. You need to set up a blog. There are quite a few free blog websites. Let me know if you can't find a good one. Your daily thoughts can be cherished by all forever. Plus, you can let everyone know everything you see in third and fourth year. Heck, you could even make a transcription of the entire Goljan audio. I am curious to ask you, why do you think that students would tell Goljan about behavioral sciences? Do you think that he actually has input on EVERY single book in the Rapid Review series? Second, don't you think most students exaggerate in terms of the breadth and scope of questions? It looks like you are keeping focused. I'm glad to see you are not steering off into something. You need this big score. You will get it. Keep up the good work. After your exam, maybe you can work on toning down your austerity.
 
p53 said:
So this made me think about other causes of dilated cardiomyopathy (cocaine, alcohol, "wet" beri beri via Thiamine deficiency (decreased ATP).


Also, viral mycocarditis (coxasachie B, and other enteroviruses), postpartum state, and ofcourse hypOthyroidism.


p53 said:
So then I got side tracked by thinking about nonenzymatic glycosylation of peripheral myelin. Conversely, if I think about diabetic peripheral neuropathy, I'll think about vincristine also causes peripheral neuropathy.

Just to add to your tangents: accumulation of odd chain FA in neuronal lipids-->peripheral neuropathy (B12 defic), but here you will also get defects in CS and PC tracts.

Tell me this, p53: to what AA is the nonenzymatic Hgb glycosylation? And, I don't think the peripheral neuropathy is due to nonenz glycosylation. I think that is due to glc-->Sorbitol (required NADPH, via Sorbitol DHase), which leads to osmotic swelling-->peripheral neuropathy (same etiology for the rentinopathy, microaneurysms, cataracts, etc). But, correct me if I am wrong.

BTW, your tangental approach is money--I try to do the same thing, often having 4-5 books open, connection pieces, whenever a lego piece comes along the way.
 
HiddenTruth said:
And, I don't think the peripheral neuropathy is due to nonenz glycosylation. I think that is due to glc-->Sorbitol (required NADPH, via Sorbitol DHase), which leads to osmotic swelling-->peripheral neuropathy (same etiology for the rentinopathy, microaneurysms, cataracts, etc). But, correct me if I am wrong.

BTW, your tangental approach is money--I try to do the same thing, often having 4-5 books open, connection pieces, whenever a lego piece comes along the way.

You are right, the Goljan Tangential approach is the way to go. I have adopted another one of his approaches. For example, I went through all of the practice nbme questions on the website (like he mentioned in his audio to find "clues" to the answer and dissected each question i.e how they ask the question, and how would changing couple things in the question stem would create a different answer. The physical diagnosis clues are "big time" on the clinical vignettes.

Hidden, I'll give you props for the correction. Keep up the good work. Now back to studying.
 
p53 said:
You are right, the Goljan Tangential approach is the way to go. I have adopted another one of his approaches. For example, I went through all of the practice nbme questions on the website (like he mentioned in his audio to find "clues" to the answer and dissected each question i.e how they ask the question, and how would changing couple things in the question stem would create a different answer. The physical diagnosis clues are "big time" on the clinical vignettes.

Hidden, I'll give you props for the correction. Keep up the good work. Now back to studying.

p53 never replies when s/he's wrong. The tangential style applies in all facets of p53's life.
 
Pox in a box said:
I'm confused. Did you take 5/21, 5/22, and 5/23 off? By the way, this is actually pretty interesting but you're going about it the wrong way. You need to set up a blog. There are quite a few free blog websites. Let me know if you can't find a good one. Your daily thoughts can be cherished by all forever. Plus, you can let everyone know everything you see in third and fourth year. Heck, you could even make a transcription of the entire Goljan audio. I am curious to ask you, why do you think that students would tell Goljan about behavioral sciences? Do you think that he actually has input on EVERY single book in the Rapid Review series? Second, don't you think most students exaggerate in terms of the breadth and scope of questions? It looks like you are keeping focused. I'm glad to see you are not steering off into something. You need this big score. You will get it. Keep up the good work. After your exam, maybe you can work on toning down your austerity.

lol, if p53 is REALLY like the way s/he is on SDN, i have a feeling that 270 step 1 won't mount to a hill of beans when 3rd year grades/comments make mention of the fact that this person is not fit for dealing with patients or other physicians.
there is the thing of "total package" that plays a part in medicine.
streetdoc
 
Pox in a box said:
p53 never replies when s/he's wrong. The tangential style applies in all facets of p53's life.

:laugh: true, good call!

p53, you never answered my question. But, I'll tell you so you can add it to your tangential blog--it's Valine.
 
HiddenTruth said:
Also, viral mycocarditis (coxasachie B, and other enteroviruses), postpartum state, and ofcourse hypOthyroidism.




Just to add to your tangents: accumulation of odd chain FA in neuronal lipids-->peripheral neuropathy (B12 defic), but here you will also get defects in CS and PC tracts.

Tell me this, p53: to what AA is the nonenzymatic Hgb glycosylation? And, I don't think the peripheral neuropathy is due to nonenz glycosylation. I think that is due to glc-->Sorbitol (required NADPH, via Sorbitol DHase), which leads to osmotic swelling-->peripheral neuropathy (same etiology for the rentinopathy, microaneurysms, cataracts, etc). But, correct me if I am wrong.

BTW, your tangental approach is money--I try to do the same thing, often having 4-5 books open, connection pieces, whenever a lego piece comes along the way.


I hate to back up p53 a little but from according to daddy robbins.

(Daddy page 1197)
"Atleat three distinct metabolic pathways appear to be involved in pathogenesis of long-term diabetic complications although the primacy of any one has not been established. These pathways include the following

1) Formation of AGE(non enzymatic)
2) Activation of PKC
3) Intracellular Hyperglycemia with disturbances in Polyol pathways.


(Daddy page 1439)
Diabetic retinopathy seems to be due to vascular damage and the production of VEGF which causes neovascularization. But the osmotic swelling might be correct for cataracts.


As always I am willing to learn if someone can present more up to date information.
 
Hmmm.....#383 looks familiar....

-----------------------------------------------------------------------

383. the mechanism of action of sibutramine?
appetite suppression,blocking central serotonin,norepinephrine reupatake
Sibutramine is a new agent used to treat obesity. It interferes with the reuptake of serotonin and NE into the presynaptic nerve terminal, thereby increasing their levels in the brain.


384. a child can use toothbrush and has imaginary friend
at what age?
4 yrs

385. deQurvein thyroiditis associated HLA?
HLA-B35

386. chronic use of this drug to treat dermatitis herpetiform may lead to metheoglobinemia?
Dapsone
387. the most common cause of vision loss in African-American population?
open-angle glaucoma
They are five times more likely to develop it than whites, due to inherited risk factors. African-Americans over 40 and people in other ethnic groups over 60 are at greatest risk for developing glaucoma
Trachoma is found in poor rural areas of most African countries and a few other areas today.
Q is about African Americans.
Cataract is the number 1 world wide cause of blindness.
African Americans suffer 5x more from Glaucoma than other counterparts.
Age-related macular degeneration (ARMD) is the number 1 cause of blindness after 60.

388. drug of choice for treatment of sleep apnea?
Protryptilline

389. what¡¯s the second messenger for muscarinic receptors?(M1?M2?M3?)

M1,M3:IP3
M2:decreased cAMP


390. the indication of use of oseltamivir?the most common side effect?
neuroaminidase inhibitors,block release of progeny virus from cells
treatment of influenzaA,B,vomiting in 1-2days that occurs with first dose and disappears with continuing of treatment,other side effects:conjunctivitis,epistaxis,abdominal pain


391. the mechanism of action of zanamivir?indication of use?
neuroaminidase inhibitors,block release of progeny virus from cells,treatment of influenzaA,B,vomiting in 1-2days that occurs with first dose and disappears with continuing of treatment,other side effects:conjunctivitis,epistaxis,abdominal pain
exacerbate pulmonary symptoms in COPD

392. what's the second messenger for histamine receptors?
H1:IP3,H2:cAMP
393. what's the second messenger for dopamine receptors?
D1, 4 and 5 - cAMP, D2 and 3 -cAMP inhibition

394. what's the second messenger for alpha(alpha-1,alpha-2) receptors?
alpha 1 IP3
alpha 2 cAMP inhibition

395. the origin of gastrinoma in Zollinger-Ellison syndrome?
a)alpha cells
b)beta cells
c)delta cells
the answer is delta cells

396. the effects of Epinephrine and Norepinephrine on TPR(Total Peripheral Resistance)?
NE:INCREASED TPR: act through alpha receptors
EP😀ECREASED TPR: act through beta receptors


397. enzyme defect in porphyria cutanea tarda?
partial loss of activity of hepatic uroporphyrinogen decarboxylase
398. enzyme defect in acute intermittent porphyria?
defeciency in porphobilinogen deaminase(another name: uroporphyrinogen I synthase)

399. which part of thalamus considered a part of limbic system?
ant thalamus
mamillary bodies..........> ant.thalamaus.........>cingula


400. which one is not a derivative of middle trunk brachial plexus?
a)median nerve
b)ulnar nerve
c)radial nerve
d)axillary nerve
upper trunk:musculocutaneus nerve
middle trunk:median,radial,axillary nerves
lower trunk:ulnar nerve


401. the origin of C cells of thyroid?
a)first pouch
b)second pouch
c)third pouch
d)4th pouch
e)5th pouch
5th pouch(Dr Carl¡¯s book)
high yield & Kaplan say 4th pouch... which forms the ultimobranchial body... (the actual origin is migration of neural crest cells).

402. a patient with aluminium toxicity presents with dyspnea.why?(the cause of dyspnea?)
Al toxicity leads to impaired absorption of P in GI tract,decreased available P leads to decreased level of 2,3DPG,abnormal tissue oxygenation causes malaise,dyspnea,muscle weakness

403. the most common clinical presentation of chronic arsenic poisoning?
neurologic symptoms predominate:burning sensation(glove-stock distribution),bilateral arm,leg weakness(pigmentation another symptom but not the most common)

404. risk factors for developing tardive dyskinesia?
Chronic use of Neuroleptis medications,CO poisoning,female sex etc also DM,old age,smoking


405. mechanism of action of nevirapine and common side effects?
anti retro viral.... nonnucleoside reverse transcriptase inhibitor...which doenot require metabolic activation..
side effect is rash ... steven johnsons syndrome

406. mechanism of action of nelfinavir and common side effects?
anti retro viral.. protease inhibitor...
side effect diarrhea... central adiposity...inslin resistance
increased levels of TG,cholestrol,lipodystrophy

407. to treat tricyclic antidepressant overdose which treatment is not effective and WHY?
a)gastric lavage
b)use of activated charcol
c)physostigmine
d)dialysis
d:dialysis
coz TCAs have a wide Vd(volume of distribution),so dialysis not effective


408. what's the difference betwen clinical presentation of NMS and serotonin syndrome?
both of them present with hyperthermia, myoclonus,rigidity, CVinstability
in addition
NMS=altered consciousness is seen
SErotonin syndrome=diaphoresis n seizures are seen


409. which of the following statistical tests is most appropriately used to evaluate the difference in the percentage of women who lose weight on a protein-sparing diet versus the percentage who lose weight on a high-protein diet?
a)paired t-test
b)ANOVA
c)chi-square test
d)correlation
e)independent t-test
chi square used to determine between frequencies in a sample


410. which of the following statistical tests is most appropriately used to evaluate the difference between initial body weight and final body weight for each woman on a protein-sparing diet?
a)paired t-test
b)ANOVA
c)chi-square test
d)correlation
e)independent t-test
A,t-test used to examine differences between means of 2 samples,this is paired t-test coz the same women are examined on 2 diff occasions
e)independent t-test:2groups of subjects are sampled on one occasion


411. an IQ test has high interrater reliability,what does it mean?
it means that the results are very similar when the test is administered by a different examiner


412. these cells contain a peripheral hyalomere and central granulomere?
a)lymphocytes
b)monocytes
c)basophils
d)neutrophils
e)eosinophils
f)platelets

platelets!


413. in a kidney donor,what changes are seen in:
1)creatinine excretion?
2)GFR?
3)plasma Cr concentration?

Cr excretion=GFR x plasma Cr concentration
GFR decreased,plasma Cr increased,Cr excretion unchanged


414. which enzyme responsible for secretion of pancreatic enzymes?CCK or secretin?
CCK responsible for pancreatic enzyme secretion
secretin for HCO3- secretion

415. Sabin-Feldman dye test used to identify this organism?
Gold standard serologic test for toxoplasmosis

416. where¨ˆs the location of folic acid and iron absorption?
yes,duodenum, according to Kaplan most of folic acid and iron absorption occurs in duodenum
417. defeciency of this factor associated with thrombosis rather than hemorrhage?
a)factor V
b)factor VII
c)factor XII
d)factor XIII

factor XII

418. intramembranous deposits are seen in which type of glomerulonephritis?

MPGN typeII
MPGN typeI:with subendothelial deposits

419. coagulation factors inhibited by proteinC?
factor V,VIII

420. which phase of cell cycle affected by tamoxifen?
G1

421. In chemotherapy,what¡¯ the only antibiotic that¡¯s cell-cycle specific?and which phase of cycle affected by this drug?
bleomycin--G2 phase

422. the indication of use of cyclobenzaprine?
centrally acting muscle relaxant

423. the indication of use of tetrahydrozoline:
conjunctival congestion?? in allergies, it's alpha-agonist

424. the first heart sound corresponds to which of the following points on an atrial pressure tracing?
a)a wave
b)c wave
c)v wave
d)x descent
e)y descent
c wave

425. the second heart sound corresponds to which of the following points on an atrial pressure tracing?
a)a wave
b)c wave
c)v wave
d)x descent
e)y descent
v wave
 
426. S4 corresponds to which of the following points on an atrial pressure tracing?
a)a wave
b)c wave
c)v wave
d)x descent
e)y descent
a wave


427. match markers for each measurement:
1)evans blue
2)antipyrine
3)inulin
4)tritium
a)measurement of total body water
b)measurement of plasma compartment
c) measurement of extracellular fluid compartment
a)measurement of total body water: antipyrine, tritium
b)measurement of plasma compartment: evans blue
c) measurement of extracellular fluid compartment:inulin
428. mutation in apoprotein CII is seen in which type of hyperlipidemia?
type1:associated with LPL dificiency or mutation in apoCII


429. Most comonly uesd calcium channel blocker in CHF?
a)nifedipine
b)amlodipine
c)isradipine
d)diltiazem
e)verapamil
amlodipine&felodipine

430. rate limiting step of pyrimidine synthesis?
aspartate transcarbamylase

431. rate-limiting enzyme of cathecholamine synthesis?
tyrosine hydroxylase

432. side effects of carmustine?
Pulmonary toxicity.
And delayed myelosuppresion
Pul.Toxicity by Bleomycin, Busulfan,MTX, Carmustine
(BBC...MaTriX (Methotrexate)
nausea, vomiting
temp. reduction in bone marrow function (anemia)

433. what¡¯s the final product of glycolysis?
pyruate aerobic,lactate anaerobic

434. rate-limiting enzyme in glycogenolysis?
glycogen phosphorylase


435. rate-limiting enzyme in gluconeogenesis?
Fructose 1-6Bisphosphatase.
Stimulated by , ATP,Glucagon, inhibited by Insulin,AMP,Fructose 2-6 Bisphosphate.
pyruate carboxylase
PEPCK

436. what enzyme difficiency is seen in heredity fructose intolerance?
Aldolase B(Fructose 1P Aldolase),
Hereditary F intolerance.
Aldolase B found in Liver and Kidney.
not evident till babay is on mother's milk.
After Fructose ingestion, Sever Hypoglycemia ( lethargic baby, diaphoresis) and Sevr Lactic Acidosis.
Fructose 1 phosphate accumulate in Liver(hepatomegaly,hyperbili,liver damage,hypoglycemia) and Proximal Tubular Acidosis (Fanconi) in Kidney.
Negative Finding...Cataract is not present, sunce fructose is not a subtrate for aldose redutace) of len.
Tx:Eliminate fructose.

437. the skeletal muscle relaxant that release histamine?
Tubocurarine

438. rate-limiting enzyme in fatty acid synthesis?
acetyl-coA carboxylase
Acetyl CoA carboxylase, needing Biotin, ATP
Activated by Insulin,Citrate, High Carb Dieat, Low fat Diet.
Inhibited by Glucagon,Free Fatty acids in Blood, High fat diet.

439. rate-limiting enzyme in HMP shunt?
G6PD
G6PD.
The great enzyme, only rate limiting step in HMP.
HMP.
Also yeilds 2 NADPH. help in Fatty acid synthesis, Keep Glutathione reduced and Oxidative killing of bacteriain PMN.
BTW, there are other ways to get Ribose 5 Phosphate with out using G6PD, is Tranketolases, and Glycolytic intermediates, F6P,Gleceraldehyde3P are used as intermediate....But they need Thiamine . Transketolases are found in RBC for your info.
Other thing to remebr is we can differentiate G6PD deficiency from Pyruvate Kinase deficiency(which give hemolytic anemia too) is that G6PD has heinz bodies , the latter does not.
heinz bodies.
In mediteranean it is fava beans.


In america it is drug induced , infections and African Americans too
440. the phase of cell cycle affected by cytarabine?
Sphase


441. enzyme difficiency in Tangier¨ˆs disease?
Familial alpha-Lipoprotein deficiency, absence of apoA
Low sr. Chol, and HDL.
High TAG,VLDL ,Chylomicron.
lArge orAnge Tonsils,
HepAtomegaly,
Neurological deficits.......
442. enzyme difficiency in Fabry disease?
alpha galactosidase
Xlinked, accumulation of cermide trihexoside, Renal failure.
443. enzyme difficiency in Hunter &Hurler diseases?
Hunter: Aim for X, Xlinked, iduronase sulfatase, NO corneal clouding and mild MR
Hurler:Alpha - L iduronase. Corneal clouding and MR.
Drawifsm. Not diagnosed in infancy.
444. drug of choice for cysticercosis?and mechanism of action?
praziquantal- increases Ca membrane permeability causing loss of calcium.
albendazole alternative treatment
445. SIADH a side effect of which drug?
a)gancyclovir
b)foscarnet
c)amantadine
d)vidarabine
vidarabine
446. the only fatty acid that¨ˆs gluconeogenic?
propionic acid
447. mechanism of action of foscarnet?
inhibits viral replication by blocking the pyrophosphate binding site of viral DNA polymerase
448. drug of choice for blastomycosis?
itraconazole choice
amphoB for severe cases
449. which chemotherapeutic drug considered a cell-cycle nonspecific drug?
a)hydroxyurea
b)etoposide
c)metothroxate
d)busulfan
busulfan:alkylating agents cell-cycle nonspecific
450. drug of choice for African sleeping sickness:CNS stage?hemolymphatic stage?
Melarsaprol,pentamidine
 
p53 said:
Hmmm.....#383 looks familiar....

-----------------------------------------------------------------------

383. the mechanism of action of sibutramine?
appetite suppression,blocking central serotonin,norepinephrine reupatake
Sibutramine is a new agent used to treat obesity. It interferes with the reuptake of serotonin and NE into the presynaptic nerve terminal, thereby increasing their levels in the brain.

and Dopamine. It has a amphetamine like structure.
BTW: Did goljan personally call you with these, or what?
 
p53 said:
Hmmm.....#383 looks familiar....

-----------------------------------------------------------------------

383. the mechanism of action of sibutramine?
appetite suppression,blocking central serotonin,norepinephrine reupatake
Sibutramine is a new agent used to treat obesity. It interferes with the reuptake of serotonin and NE into the presynaptic nerve terminal, thereby increasing their levels in the brain.


Why?
 
I know him about as well as I know you. Although, he is doing some WAY deep searches of my old posts (like 200 ago)
 
Some people will never figure out when they are being helped. You know, I could have NOT posted generic review questions (that anyone can find on the internet) that I consider to be helpful for any medical student's "broad medical knowledge."

Makes you wonder how much other stuff that is not found in any review books but turns out to be high yield from p53's posts.
 
p53 said:
Some people will never figure out when they are being helped. You know, I could have NOT posted generic review questions (that anyone can find on the internet) that I consider to be helpful for any medical student's "broad medical knowledge."

Makes you wonder how much other stuff that is not found in any review books but turns out to be high yield from p53's posts.

I bet you heard about humility in the sermon this morning. Thanks for that random deep thought.
 
I could not believe it. Just took the NBME form A exam in simulation mode and scored a 770. This sets me up pretty good psychologically for next week 😀

Since I am such a nice guy that doesn't hold grudges, if there are any people that have taken NBME form A and have any lingering questions about the concepts tested you may post it here while it is still fresh on my mind. For those that have more than 4 weeks until the exam, I HIGHLY recommend doing just the pathology questions in BSS (Board Simulator Series) by our friend Goljan. Goljan's explanations on BSS Pathology is PURE GOLD. It will drill the most important pathology concepts from his audio in your head forever. There is nothing like doing questions to test your mastery of a concept by Goljan to see if you really understood his audio. Many of the high yields (100 page notes and audio) are in his BSS questions (I read all of the explanations even the ones that I got right) ! Now you know why people that do BSS score so high. It is because of Dr. Goljan!

The last leg of my march will be spent on First Aid that is well fortified with all of Goljan's nuggets from BSS, and his 100 page notes.
 
p53 said:
I could not believe it. Just took the NBME form A exam in simulation mode and scored a 770. This sets me up pretty good psychologically for next week 😀

Since I am such a nice guy that doesn't hold grudges, if there are any people that have taken NBME form A and have any lingering questions about the concepts tested you may post it here while it is still fresh on my mind. For those that have more than 4 weeks until the exam, I HIGHLY recommend doing just the pathology questions in BSS (Board Simulator Series) by our friend Goljan. Goljan's explanations on BSS Pathology is PURE GOLD. It will drill the most important pathology concepts from his audio in your head forever. There is nothing like doing questions to test your mastery of a concept by Goljan to see if you really understood his audio. Many of the high yields (100 page notes and audio) are in his BSS questions (I read all of the explanations even the ones that I got right) ! Now you know why people that do BSS score so high. It is because of Dr. Goljan!

The last leg of my march will be spent on First Aid that is well fortified with all of Goljan's nuggets from BSS, and his 100 page notes.


Man what a score!!! hahah craazy man. I got a couple questions:

1) What u think about questions where u have goljan saying one thing, and First Aid saying another? For example, common metasasis to liver is colon in First Aid, but Goljan says lung is. Another one from the NBME A test was about the IV drug user who gets endocarditis and lung problems. Goljan says lung problems and IV drug abuse = cryptococcus, First Aid says Candida. So whats your thoughts on that?

2) What is your approach when doing these questions? Do u just know it from knowledge or are u carefully dissecting the question or just looking at the answer choices. Getting a 770 is knowledge but test taking skills must be good. So if u could give us some tips on what u do would help alot of us.

If anyone else has somehting to say about these questions, please feel free to share!

By the way p53, i think the advice on the BSS is golden. Too late for me to do it, but the MS2s can definetly benefit. Great work. U are still pretty wack though 😀
 
p53 said:
I could not believe it. Just took the NBME form A exam in simulation mode and scored a 770. This sets me up pretty good psychologically for next week 😀
Sounds like you're gonna rock it. 👍
 
omarsaleh66 said:
By the way p53, i think the advice on the BSS is golden. Too late for me to do it, but the MS2s can definetly benefit. Great work. U are still pretty wack though 😀

p53 has some bolts loose in the personality department but that is an awesome score if true. I guess he is going to be this years SDN usmle MVP.


What is the ISNB number for the BSS you guys are talking about is it the one that is $99??? I saw several books on amazon but could not find the one with goljan?? Thanks
 
omarsaleh66 said:
Man what a score!!! hahah craazy man. I got a couple questions:

1) What u think about questions where u have goljan saying one thing, and First Aid saying another? For example, common metasasis to liver is colon in First Aid, but Goljan says lung is. Another one from the NBME A test was about the IV drug user who gets endocarditis and lung problems. Goljan says lung problems and IV drug abuse = cryptococcus, First Aid says Candida. So whats your thoughts on that?

Neither, the answer was aspergillois. http://hivinsite.ucsf.edu/InSite?page=kb-05&doc=kb-05-02-02

The key was bilateral infiltrates, and the size of the fungus was 1 cm (candida ) has large vegetations. Also, the hemoptysis which should clue you in that it was a preexisting cavitation of TB inhabited by aspergillois.

Omar, you are a smart guy, I can tell from your posts. The key for you is to not take anything for granted. For example, you mentioned Candida and Crypto. However, you dismissed the other diagnostic clues. ON EXAM DAY, PAY VERY CLOSE ATTENTION TO ALL PHYSICAL DIAGNOSTIC FINDINGS. As Goljan would say they don't give you fluff so go slow. You will be fine on the exam, trust me. Just go slow and concentrate. The way exam makers trick sharp students is to put them to sleep and make them think it was an easy question. Don't be duped.

The right answer for the liver met question is Lung. This was also verified at the UAB Pathology website that has the pathology slide set that Goljan keeps mentioning in his audio. Move on down to the gross picture of liver.

http://peir2.path.uab.edu/pdl/dbr.c...view_records=View+Records&view_records=Search
 
chak_de_phatee said:
p53 has some bolts loose in the personality department but that is an awesome score if true. I guess he is going to be this years SDN usmle MVP.


What is the ISNB number for the BSS you guys are talking about is it the one that is $99??? I saw several books on amazon but could not find the one with goljan?? Thanks

Hey man, its like 5 books with like 700q per book or somehting. yeah thats probably it. What u can do though, is look up board simulator series on amazon. The newest results will pop up first. Maybe scroll down and get some of the older edition books for much cheaper. Maybe u can get the BSS cd off ebay or something. Goljan is one of the writers. BSS is written by multiple contributers.

later
 
Don't forget when you go to the bookstore on Monday to ask for the series that was published in 1997 (which means it was ACTUALLY WRITTEN in 1994(since my calculations have Goljan's audio verifying that his biochemistry book was published three years after the lectures). If you're scared of old books (and the questions are pretty tough so they frustrate a lot of people), you might want to steer clear.
 
If you like his audio, you would be a hypocrite to not like his BSS Pathology questions because they are the same. In the audio, he said "Hey I just thought about this, a good question for the boards would be a person's vision keeps changing as for someone with Diabetes.' That exact question was in BSS. In fact he even had a question about CALLA antigen for ALL in his BSS questions even though he said he just put it into his high yield. The man has taught pathology for USMLE for 20+ some years, do you honestly believe 40 hours of lecture is from just his 2001 students?

This is why savvy students that like Goljan use his 1999 pathology book because it has the same information as his audio in PROSE form. Shelf life for information in Pathology is overrated. On the other hand, it would be stupid to study immunology, pharmacology, and molecular biology from a book in the 90's.

Ask your best friend Hidden which Goljan book he used as his main resource. It isn't the 2004 Rapid Review. Nuff said.
 
p53 said:
Neither, the answer was aspergillois.

The key was bilateral infiltrates, and the size of the fungus was 1 cm (candida ) has large vegetations. Also, the hemoptysis which should clue you in that it was a preexisting cavitation of TB inhabited by aspergillois.

The key for you is to not take anything for granted. For example, you mentioned Candida and Crypto. However, you dismissed the other diagnostic clues. ON EXAM DAY, PAY VERY CLOSE ATTENTION TO ALL PHYSICAL DIAGNOSTIC FINDINGS. As Goljan would say they don't give you fluff so go slow. You will be fine on the exam, trust me. Just go slow and concentrate. The way exam makers trick sharp students is to put them to sleep and make them think it was an easy question. Don't be duped.

wow i didnt even think about that! See, this is the thought process for people getting high scores. Most students (especially me) do fall into these traps and get fatigued and select "buzz" words. Thanks alot for your insight man; I really appreciate it. Definietey gotta think more like u said. Great tips.

peace
 
p53 said:
If you like his audio, you would be a hypocrite to not like his BSS Pathology questions because they are the same. In the audio, he said "Hey I just thought about this, a good question for the boards would be a person's vision keeps changing as for someone with Diabetes.' That exact question was in BSS. In fact he even had a question about CALLA antigen for ALL in his BSS questions even though he said he just put it into his high yield. The man has taught pathology for USMLE for 20+ some years, do you honestly believe 40 hours of lecture is from just his 2001 students?

This is why savvy students that like Goljan use his 1999 pathology book because it has the same information as his audio in PROSE form. Shelf life for information in Pathology is overrated. On the other hand, it would be stupid to study immunology, pharmacology, and molecular biology from a book in the 90's.

Ask your best friend Hidden which Goljan book he used as his main resource. It isn't the 2004 Rapid Review. Nuff said.

Who are you talking to, MVP? You probably struggled on the verbal reasoning section of MCAT. I didn't say I wasn't using BSS nor did I say I was. I just said it was written mid-90's. Of course they are the same (the audio and BSS). If not, he'd be suffering from split-personality. There should be very little discrepancy between BSS, the audio, Rapid Review, and the scribbles in Idiopathic's notebook. You're silly.
 
Pox in a box said:
Don't forget when you go to the bookstore on Monday to ask for the series that was published in 1997 (which means it was ACTUALLY WRITTEN in 1994(since my calculations have Goljan's audio verifying that his biochemistry book was published three years after the lectures). If you're scared of old books (and the questions are pretty tough so they frustrate a lot of people), you might want to steer clear.

Are the path q's in one book, or is at all spread out based on systems? I've heard that the series is actually not that great.
 
Pox in a box said:
Who are you talking to, MVP? You probably struggled on the verbal reasoning section of MCAT. I didn't say I wasn't using BSS nor did I say I was. I just said it was written mid-90's. Of course they are the same (the audio and BSS). If not, he'd be suffering from split-personality. There should be very little discrepancy between BSS, the audio, Rapid Review, and the scribbles in Idiopathic's notebook. You're silly.

Pox, I am not going to take this personal because you are frustrated with your NBME performance. If you ask for help, I will give it to you. No grudges.

Furthermore, I will pray to God that you have an exam that is loaded with Pathology because if you don't you might be in for a long day. I truly want you to do well, now go study and kick some butt next week.
 
p53 said:
Pox, I am not going to take this personal because you are frustrated with your NBME performance. If you ask for help, I will give it to you. No grudges.

Furthermore, I will pray to God that you have an exam that is loaded with Pathology because if you don't you might be in for a long day. I truly want you to do well, now go study and kick some butt next week.

Take what personal? I've kicked butt on every NBME exam I've ever taken (except a bit below avg. on biochem)...thanks for the motivation though.
 
p53 said:
I could not believe it. Just took the NBME form A exam in simulation mode and scored a 770. This sets me up pretty good psychologically for next week 😀

Since I am such a nice guy that doesn't hold grudges, if there are any people that have taken NBME form A and have any lingering questions about the concepts tested you may post it here while it is still fresh on my mind. For those that have more than 4 weeks until the exam, I HIGHLY recommend doing just the pathology questions in BSS (Board Simulator Series) by our friend Goljan. Goljan's explanations on BSS Pathology is PURE GOLD. It will drill the most important pathology concepts from his audio in your head forever. There is nothing like doing questions to test your mastery of a concept by Goljan to see if you really understood his audio. Many of the high yields (100 page notes and audio) are in his BSS questions (I read all of the explanations even the ones that I got right) ! Now you know why people that do BSS score so high. It is because of Dr. Goljan!

The last leg of my march will be spent on First Aid that is well fortified with all of Goljan's nuggets from BSS, and his 100 page notes.

I am glad to see your brain is as big as your mouth....congrats on the 770.
 
HiddenTruth said:
Are the path q's in one book, or is at all spread out based on systems? I've heard that the series is actually not that great.
They are spread out based on the system that the book is covering, but if you get the disk you can select to do all the path Qs (~600) in one sitting since the disk I had was unable to keep track the Qs done.
 
Idiopathic said:
If Gross Anatomy is what kept you from your goal, then you either knew nothing about Gross Anatomy or you weren't very far off from your goal.

Even though p53 is a pompous toolbag at times, he/she actually posts legit information in regards to actual Step 1 studying. I don't recall seeing anything that hasn't checked out. This post by p53 is actually pretty good. I did a lot of p53's strategy but a lot different as well. As soon as my surgery rotation is over, I'll post what I did for the future generation of test takers.
 
Pox in a box said:
Even though p53 is a pompous toolbag at times, he/she actually posts legit information in regards to actual Step 1 studying. I don't recall seeing anything that hasn't checked out. This post by p53 is actually pretty good. I did a lot of p53's strategy but a lot different as well. As soon as my surgery rotation is over, I'll post what I did for the future generation of test takers.

Look I took the test too, you know. I had about three questions that could not be answered from a cursory knowledge of GA. I cannot imagine more than ten legitimately difficult GA questions on one exam is all.
 
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