My strategy failing me?

When I first started thinking about the Step 1, I was a bit worried about microbiology.  This was partly because I didn't need to know much as part of my coursework, and partly because microbiology was the bane of my existence during undergrad.  So, about six months ago, I spent a couple of days reading Levinson and making notes into First Aid.  At that time I felt I'd learned heaps, but I finally began revising it today.

As I was reading through, I thought, "Wow, this isn't quite as bad as I'd remembered."  Then, I started doing Kaplan questions.  Mother of god.  I got 46% correct on the first question block.  46%?!?  How can this stand?

The thoroughly abrading thing about all of this is that most of the questions I got wrong were related to things I have never before seen!  Did you know Pseudomonas aeruginosa has two elastases called LasA and LasB responsible for ecthyma gangrenosum?  I sure didn't until today.

Did my high-yield review resources let me down?  Or does Kaplan just suck?  Either way, are they preparing me adequately for the USMLE or am I being led into a dark alleyway for mental assault and battery?

Feeling crotchety, --KM

How studying is (or is not) going so far ...

So it's taken me two weeks to tackle my "tough subjects" of biochemistry, pharmacology, and embryology.  (I threw in a bit of path last week just to keep myself sane.)

I will start with Embryology because it turned out to be way better than I was expecting.  Basically we all start out as a little ball.  Then that ball gets squished into a pancake.  Then the pancake splits up into three layers and we fold up into a mushroom.  In the mushroomation embryo phase, there is a big groove all the way down the back which gets "zipped up".  If the fly stays down, it = neural tube defect. If something goes wrong at the head, you get anencephaly.  If something goes wrong at the bum, you get a myelomeningocoele.  Either way, it sucks.  Also, the pharyngeal pouches - funky ruffles on your cheeks that kind of look like Captain Hook's shirt, and turn into your ears and face and stuff. 

Oh yea, and your heart, thyroid gland, and pituitary all start in the mouth.  Weird as!

Anyway moving on.

Biochemistry is rough for me.  I really struggle with remembering the names of enzymes, and all of the lysosomal storage diseases sound the same to me!  I made awesome flash cards, which have helped a little bit, but I still find that I second-guess myself when I'm answering practice questions.  I worked on biochem for several days, but I just had to leave it and move on.

Pharmacology would be easy if it were just remembering the drugs.  I am really good at mechanisms of action, overdose/withdrawal and all of that.  What I suck at is anything involving a graph.

**PREPARE FOR RANT**

Seriously, the person who decided that those stupid graphs of heart rate and blood pressure with sympathetic antagonists/agonists were a good idea can eat shit and die as far as I'm concerned.  Why the hell would I care about a hypothetical experimental antagonist that is never used except for USMLE questions?  So it tests knowledge of receptors and crap?  Who the fuck cares!  Is it clinically useful? I think not. *Le sigh* 

ALSO - the next Lineweaver-Burke plot I see may drive me into a hysterical fit.  If they ask me a question about enzyme affinity and reaction rates in words I am fine, but as soon as it is in a graph - it's like a kaleidoscope of weeping, uncontrollable swearing, and inappropriate laughter!  People may think I have the "Happy Puppet" Angelman syndrome!  (See, I did learn something studying that biochemistry crap.)

Anyway, it took me two weeks but I did manage to survive the subjects that I really suck at.  Today I will do behavioural sciences and make a start on micro.  Wish me luck!

Boot camp begins!

Well, school is finally over.  Which means I have 6 weeks to do some hardcore USMLE study!  EEK!

I have read all of First Aid this year and added some extra notes.  From the study and practice questions I have done so far, I have realized the areas I need the most work on are biochemistry, embryology, and pharmacology.  So I'm going to focus on really studying those areas for the first week, and then again at the very end.  The rest of my study is going to be practice questions, practice questions, practice questions!!  I have already done a few questions in Kaplan Qbank and First Aid Q&A, so I'm going to keep using those until I feel really confident about my question-answering strategy.  Then I am going to start UWorld - for the ultimate power study of awesome!

It is really crunch time! --KM <3

Mixed acid-base disorders

Epiphany today!

You know how CO2 and bicarbonate levels change together?  Like if CO2 goes up, bicarb goes up, and if CO2 goes down, bicarb goes down?

Well, then: LET ME BLOW YOUR MIND!

In mixed acid-base disorders, there is both a respiratory and a metabolic acid-base disruption.  So the bicarb and CO2 change in opposite directions!


It totally makes sense if you think about it a little bit.  For example, in cardiopulmonary arrest, the patient stops breathing.  They will therefore accumulate CO2 and have a respiratory acidosis.  BUT because they stop breathing (and cause they're ludicrously ischaemic from no heart pumping), they also become hypoxic.  Anaerobic metabolism ensues and lactic acid accumulates.  They will then develop a metabolic acidosis, saturating all the available bicarb with a proton blitz - leading to a mixed acidosis which messes with everyone's minds.

Holy crap! Amazing.

EEK! Scheduled today!

I finally picked a date today!  28 December 2010!  I'm so nervous/excited!

Meanwhile, school is dominating my life and I have had basically zero time to do proper USMLE study :(  I am hoping to be back on track by the end of this week.

It is so annoying to have to study for 80 gajillion things all at the same time!  Grr....

Acid-base: My Achilles' Heel

ACID-BASE BALANCE IS THE BANE OF MY EXISTENCE!!!

There are not very many things in this life that I naturally suck at.  Basically the list just includes team sports and acid-base balance. 

My strategy for overcoming this obstacle has thus far been identical to my strategy for dealing with team sports: complete and utter avoidance.  Unfortunately, acid-base keeps poking its' ugly snout back into my USMLE business, and I realize I must meet this enemy head-on (or risk having my ass handed to me on a platter on test day).

To date, physiology textbooks like Sherwood and Guyton (both my usual favorites) have failed me dismally.  So it is with a heavy heart that I turn to USMLE Step 1 Secrets in the vain hope that somehow this high-yield review source will explain the mysteries of protons and bicarbonate in such a way as my currently feeble mind can unravel.

God's teeth!  What witchery be this?  It is starting to make sense! (Just a little bit.)

Stuff I didn't know until now:
- The kidney is 'better' at excreting bicarbonate than it is at retaining it.  This explains why renal compensation in respiratory alkalosis (compensatory mechanism = excrete bicarb) is faster and more complete than the renal compensation for respiratory acidosis (compensatory mechanism = retain/synthesize bicarb).

- There are a gajillion things that can cause metabolic alkalosis, but they all revolve around a couple of major mechanisms:

1. Hypokalaemia: three main effects ...
   (1) ↓ K+ secretion at distal tubule --> ↑ H+ loss at distal tubule (serum pH ↑s)
   (2) Cells exchange K+ for H+ --> ↓H+ in serum and ↑H+ in cells (serum pH ↑s)
   (3) Proximal tubule cells excrete excess intracellular proton in the form of ammonium ion (serum pH ↑s)
2. Excessive activation of aldosterone receptor - promotes K+ & H+ excretion in exchange for Na+ retention (serum pH ↑s through direct effect of excreting protons and indirect effect of hypokalaemia)
3. Volume depletion - causes ↑ Na+ retention (attempt to maintain plasma volume) --> ↑H+ loss and ↑bicarb retention at proximal tubule; also indirect effects of RAAS --> ↑ aldosterone activity
4. Proton loss to the outside world - loss of acid to outside world --> ↑ serum pH

So, things that cause metabolic alkalosis include:

• Loop & thiazide diuretics - vol depletion & hypokalaemia
• Bartter syndrome - loss of Na+/K+/2Cl- transporter - mimics loop diuretic
• Gitelman's syndrome - loss of Na+/Cl- transporter - mimics thiazide diuretic
• Vomiting & antacid overuse - loss of acid
• Conn's syndrome - primary hyperaldosteronism
• Cushing syndrome - excess glucocorticoid exerts effect on aldosterone receptor
• Liddle's syndrome - mimics hyperaldosteronism
• 11β-hydroxycortisol dehydrogenase deficiency (essential or secondary to licorice) - decreased breakdown of steroids - mimics hyperaldosteronism

I think it's better to learn the mechanisms than to memorize the list.

Metabolic acidosis coming up soon!  Stay tuned ...

Xo --KM <3

Pre-renal vs. Intra-renal Ischaemia

Holy crap - busiest month ever.  I srsly don't know where the last month went.  It just disappeared. :S

USMLE studying has basically gone out the window lately.  :( But I am trying to get back into it with renal!  Renal physiology is kind of meh but the pathology is amazingly cool.

Acute tubular necrosis is the commonest intra-renal cause of acute renal failure.  It can be caused by toxins or ischaemia.  At first this seemed straightforward to me, but then I realized that pre-renal acute renal failure is ischaemic.  This caused me to question, how in the &$%! do you tell the difference between intra-renal ischaemic acute renal failure and pre-renal ischaemic acute renal failure??

Apparently it goes like this:

Pre-renal: renal cells are hypoperfused, but tubular function remains intact!  Tubule cells increase reabsorption of sodium, and urea is retained in the medulla.  This is an attempt to create concentrated urine and maintain plasma volume (...and thereby maintain perfusion).
-BUN/Creatinine ratio (quick and dirty, but not specific): Elevated >20:1
-Fractional excretion of Na+ (more specific measure .. basically the clearance of sodium weighted by creatinine clearance): Reduced <1%

Intra-renal: renal tubule cell function is impaired!  Sodium and urea cannot be reabsorbed.
-BUN/Creatinine ratio: Reduced <10:1
-FENa+: Elevated >2%

Also, toxins which can cause ATN:
"Color, contrast, and chemo"
= Heme pigments (Hb and Mb) 
= Radiography contrast media 
= Chemotherapeutic agents: cisplatin, aminoglycoside A/Bs, & Amphotericin B