Studying for the boards overwhelms most people. The sheer amount of information to know is staggering. And while being a good doctor will require you to know much more than what is covered on a shelf exam, the USMLE steps, or the COMLEX, you don’t have to know everything to do well on the standardized exams you’ll take during your medical training.Have you ever heard of the Pareto principle? The economist, Vilfredo Pareto, observed that 20 percent of the pea plants in his garden produced 80 percent of his crop. Also called the 80/20 law, Pareto noticed and applied this phenomenon to other areas of life (80 percent of wealth is held by the richest 20 percent of people, 80 percent of a company’s profits comes from 20 percent of its products, etc.). I would argue that this principle can be applied to your board preparation as well. Put most generally, the Pareto principle may be stated in terms of 20 percent of your effort is responsible or 80 percent of your achievement.
Wait a minute. Am I saying that eighty percent of your USMLE Step 1 score will come from just 20 percent of the testable concepts you study? Yeah, pretty much. Or to put it differently: 20 percent of your study and effort will account for 80 percent of your success.
Let me be clear, I’m not saying you should only study 20 percent of your First Aid for the USMLE or complete only 20 percent of the USMLE World or ExamGuru Qbank you purchased. But I am saying there are two lessons you can learn from the Pareto paradigm: 1) learn to know when you should cut your losses when studying a given topic and 2) invest your time in learning the most important material for a given topic.
We’ll take the second lesson first. Consider a highly complex topic: steroidogenesis. You could memorize the entire steroidogenesis pathway, noting the molecular structure of each substance, the enzyme responsible for converting the substance into its product, the mechanisms of action of each molecule, the clinical consequences of a deficiency or excess of a given substance within the multiple pathways, the derangements in a patient’s metabolic panel that would occur when a given enzyme is knocked out, drugs which block certain enzymes in the pathway, etc. There’s a lot. And if you’re an endocrinologist, knowing all this in all its glorious detail is probably necessary. But if you’re a second-year medical student about to take your first licensing exam, the detail could be your downfall.
There are nearly 30 individual enzymes and substances on the steroidogenesis pathway (some with multiple names). If you were about to take your board exam in 5 minutes, and asked me what you needed to know, I would tell you to remember six things (about 20 percent, get it?):
1. 21-Hydroxylase converts progesterones (progesterone and 17a-hydroxyprogesterone) into steroids with weak mineralocorticoid and glucocorticoid activity.
5. Without mineralocorticoids a person will not be able to take up Na+ and excrete K+ and without corticosteroids, gluconeogenesis suffers.
6. Excessive androgens (androstenedione and testosterone) as in the case of 21-hydroxylase deficiency will virilize a female fetus due to the extra male sex hormones. She will likewise suffer from hyponatremia and hyperkalemia (because of absent aldosterone) and hypoglycemia (from absent cortisol). A male fetus will not suffer from ambiguous genitalia but will have the metabolic derangements.
If you understand the above six ideas, I would argue that you will get 80 percent of the questions related to steroidogenesis correct on your board exam. The six facts I wrote above give you all you need to know to understand and choose the correct answer for questions related to congenital adrenal hyperplasia’s pathophysiology (deficient 21-hydroxylase for the majority of cases), metabolic consequences (salt-wasting, with hyponatremia and related hypotension, hyperkalemia, and hypoglycemia), clinical manifestations (ambiguous genitalia in female) and diagnosis (elevated serum 17a-hydroxyprogesterone, the immediate precursor used by 21-hydroxylase to make the intermediary steroids that will in turn become aldosterone or cortisol). However, these six facts will also help you derive the answer to questions about excess mineralocorticoids (hypernatremia, hypokalemia) as occurs in primary hyperaldosteronism (Conn syndrome) or a deficiency in mineralocorticoids as occurs in Addison’s diseases (which also and primarily causes a deficiency in cortisol).
Now I know there’s more to steroidogenesis and congenital adrenal hyperplasia than just the above six facts. You’ll ask, what about cases of CAH caused by 17-alpha-hydroxylase or 11-beta-hydroxylase? I would respond: know thyself. To go back to the lessons of Pareto’s paradigm: know when to cut your losses. If you’re the type of person who always seems to “mix up” the differences amongst the three most often mentioned causes of CAH, then ignore two of them and tell yourself that you are only going to be responsible for knowing all you can know about 21-hydroxylase deficiency.
On exam day, you might encounter a case of CAH and get asked about which enzyme is the most likely cause. Even if the question writer intended the vignette to point toward a 11-beta-hydroxylase deficiency as the answer. If you know the details about 21-hydroxylase deficiency, you’ll at least be able to rule out 21-hydroxylase deficiency as the correct answer and improve your odds of a correct guess. You know what else you’ll do? By knowing the specific topics where you should cut your losses, you’ll give yourself permission to relax and will prevent yourself from getting confused by vain efforts at trying to know everything.
Now, don’t you feel better when you read something like this:
A newborn infant is examined in the delivery room and found to have ambiguous genitalia. Non-invasive prenatal testing was performed at 11 weeks gestational age and the results showed a karyotype consistent with a female fetus. Physical examination of the infant shows clitoromegaly and partial fusion of the labial folds. The infant appears otherwise well with normal vital signs. Which of the following is the most likely mechanism involved?
A. Androgen receptor defect
B. Complete gonadal dysgenesis
C. Deficiency of 21-hydroxylase
D. Ovarian failure
E. Prenatal androgen exposure
Maybe Gregor Mendel and Vilfredo Pareto were onto something with their little Pisum sativum plants. Maybe in that plant lies the key to all original insights. So you could either cultivate a pea garden yourself and hope it leads to a breakthrough insight like it did for Pareto or Friar Mendel (being known to history as the “Father” or “Mother” of Board Exam Preparation wouldn’t be so bad, would it?) or you could just rely on Pareto’s insights (well, I guess, Mendel’s too for some genetics stuff) to provide the shortcut to your own intellectual breakthroughs. All I’m saying is give it a try. Approach your board preparation with intentionality and intellectual humility, and you’ll reap the rewards.