How to Answer Board-Style Multiple-Choice Questions Like a Boss

From Gomerblog http://gomerblog.com/2014/05/medical-specialty

The multiple-choice question (MCQ) is the workhorse of medical education. All of the major testing stakeholders (National Board of Medical Examiners, American Board of Medical Specialties, etc.) use MCQs to make major promotion and licensing decisions. So, it’s important to understand how to answer MCQs accurately and efficiently.

Let's review how to approach board-style MCQs. Because they’re so heavily scrutinized, these MCQs tend to be bulletproof against the hacks that unravel poorly written questions. However, a strategic approach to MCQs can help you apply your knowledge to achieve the score you deserve.

First, some definitions are imperative. MCQs consist of a stem and options. The options consist of several distractors and one correct answer (highlighted yellow in this blog).

In normal lung physiology, which of the following gases is exchanged across the alveolar membrane? [stem]  

A. Oxygen [answer]  

B. Helium 

C. Methane

D. Radon 

E. Chloroform

First, look at the stem, and ask yourself, “is the material in the stem needed to answer the question?” Board-style MCQs infamously include an exhaustive case presentation with extraneous history, exam, and lab data. With an average time allotment of only 2 minutes per question, it may be helpful to ignore anything you don’t need. In the following question, the options have no relationship with the stem, so looking at the options first can save a lot of time:

A 62-year-old man presents with acute, substernal chest pain. Physical exam reveals diaphoresis and bibasilar crackles. Serum troponin is 20 ng/ml and EKG reveals ST-segment elevation in leads V2–V6. Which of the following is a risk factor for coronary artery disease?  

A. Cigarette smoking 
B. “Type B” personality
C. Diet rich in fruits and vegetables
D. Excess water intake
E. Regular exercise 

Second, look at the options, and ask, “are the distractors plausible?” Board-style MCQs usually supply reasonable options, but the list is often easily reducible to 2-3 likely possibilities. In this question, only one of the options could reasonably be correct, at least by the standards of modern medicine:

Which of the following is the MOST EFFECTIVE treatment for an acute gout attack?

A. Purging
B. Bleeding
C. Moxibustion
D. Radioactive waters
E. Colchicine 

Third, ask “are the options homogeneous?” Asymmetric options are rare in board-style MCQs, but differences in option length, verb tense, and number agreement can alert you to distractors. In this question, the longest option, which includes a singular response to match the singular question (“next test”), is correct:

A 23-year-old woman with no significant medical history presents to the emergency department with sudden-onset, severe headache. Blood pressure is 186/102, heart rate is 56, and temperature is 38.6°C. Funduscopic exam reveals mild papilledema. The most appropriate NEXT TEST would be
A. WBC count
B. Head CT, followed by lumbar puncture if no mass lesion is found
C. Frequent neurologic exams
D. Cranial decompression
E. Antibiotics 

Finally, again considering the options, ask yourself, “did I avoid superlatives?” Options that contain “always,” “never,” “all,” or “none” are frequently distractors because the absolute nature of these terms doesn’t match the real-life uncertainty of clinical medicine. On the other hand, descriptors such as “usually normal” may be too vague to be listed in a correct answer:

A 19-year-old woman notes a malar, photosensitive rash and wrist arthralgias. Heart and lung exams are normal. White blood cell count is 2.6 K/mcl, hemoglobin is 9.2 g/dl, and platelets are 36 K/mcl.

A diagnosis of lupus is MOST LIKELY in this patient for which of the following reasons?

A. Malar rash is always diagnostic of lupus.
B. Pancytopenia may be associated with lupus.
C. Pulmonary exam findings are never normal in lupus.
D. Joint exam findings are usually normal in lupus.
E. All of the above.

While these strategies can’t substitute for true understanding, they may help you avoid some common pitfalls in answering MCQs. Good luck on the boards!

 “Superficially, it might be said that the function of the kidneys is to make urine; but in a more considered view one can say that the kidneys make the stuff of philosophy itself.” 

-- Homer Smith, Lectures on the Kidney, 1943

More Reading
How to Construct Multiple Choice Questions
NBME Constructing Board Questions
Effectively Writing Questions
Another good review on writing questions

James Novak
Nephrology Program Director
Henry Ford Hosptial

NSMC Intern Class of 2018

Hypocalcemia - What's the diagnosis - Answer

This was an interesting case. A woman with a previous history of hyperparathyroidism and multiple neck surgeries who developed severe, symptomatic hypocalcemia 3 hours following a parathyroidectomy was thought to have failed because of a persistently elevated PTH level. This suggests that did in fact successfully remove her parathyroid gland and that there was an issue with the assay.

In the hospital referred to in this case, the assay used was a Roche Elecsys PTH STAT assay. This is an antibody-based assay that uses two murine antibodies - a "capture" antibody and a "signal" antibody. In patients who have been previously exposed to murine tissue, anti-mouse antibodies can be present in the serum that bind to both of these antibodies giving a false positive result on the assay. In this case, the patient had received OKT3 in the past which has been associated with a prevalence of anti-mouse antibodies of up to 26%. Her PTH level was repeated using an alternative assay - her pre-op PTH was 18 pg/ml and her post-op PTH was 5 pg/ml. Unfortunately, she required long-term treatment with vitamin D and calcium supplementation. In retrospect, the normal calcium and phosphate in a patient with this degree of apparent hyperparathyroidism and normal kidney function was a clue that there may have been an issue with the test although, of course, it is easy to say that knowing the answer.

Congratulations to "anonymous" for getting the correct answer. The complete case report can be found here.

Hypocalcemia - What's the Diagnosis?

A 36yr old woman with a history of PCKD was referred for surgical treatment of hyperparathyroidism. She had a history of two prior failed kidney transplants following which she had been on dialysis for more than 10 years. She had a third renal transplant 10 years prior to this presentation which was still functional. At the time of her transplant, she had received OKT3 and was currently maintained on tacrolimus and prednisone. She had a long history of hyperparathyroidism. Six years prior to her transplant, she had a subtotal (3.5 glands) parathyroidectomy. The year of her transplant, she had another neck exploration with the removal of 8 nests of hypercellular parathyroid tissue.

At the time of this presentation, her PTH was 3,300 pg/ml despite treatment with cinacalcet. Her ionized calcium was normal (1.2 mmol/L) but she complained of poor concentration, fatigue and depression. Serum phosphorous and creatinine were normal. She had a normal sestamibi scan but an US revealed hyperplastic parathyroid tissue in her neck.

During the parathyroidectomy, frozen section revealed hypercellular parathyroid tissue that was removed. However, pre-op, intra-op and post-op PTH levels were elevated at >1700 pg/ml. Because of the persistently elevated PTH, it was considered a failed operation and calcium supplementation was not started post-op. However, within 3 hours of the operation, she developed perioral numbness, tetany and muscle spasms in her legs. Her ionized calcium was low (0.9 mmol/L) and her symptoms resolved after treatment with iv calcium. Her PTH remained elevated at 3000 pg/ml.

What is the reason for her acute hypocalcemia in this setting? Answer in the comments please.

Kidney Stones - What's the diagnosis? - Answer

This was an interesting case and all those who responded correctly identified that the patient had bowel pathology. However, only one person figured out that the issue was an ileostomy. This patient had a low urine volume and an extremely low urinary citrate and sodium. The low citrate could indicated a renal tubular acidosis except that the urinary ammonium was high and the urine pH was very low indicating preserved ability to acidify the urine. This points to a metabolic acidosis. The urine sodium in an average US resident is between 100-200 mmol/day. Outside of the amazon, it's hard to imagine that anyone could take in this little salt. This points towards loss of sodium bicarbonate and water from the GI tract.

Finally, in the setting of IBD, generally it is accompanied by hyperoxaluria. There are a number of potential mechanisms for this; decreased metabolism of oxalate by oxalobacter formigenes, decreased calcium binding to oxalate because of the relatively increased binding of calcium to malabsorbed fat in the GI tract. In any case, in order to have hyperoxaluria, it is necessary to have a functioning large bowel. In this case, the patient's urinary oxalate was 28 which is in the low normal range and not suggestive of hyperoxaluria. Thus, the diagnosis is high output of alkaline fluid from an ileostomy.

The treatment in this case is to increase fluids and treat with a combination of sodium and potassium citrate. Even a small rise in urine pH would significantly reduce the risk of uric acid stones while the citrate and increased volume should reduce the calcium oxalate stone risk.

Kidney Stones - What's the diagnosis?

A 65yo man was reviewed in the clinic for assessment of kidney stones. He has a history of stones for at least 8 years and has been passing small calculi on a regular basis for the last few months. His 24 hour urine results are shown below (results are 24 hour total values unless otherwise specified):

Volume, Liters	0.71	Sodium, mmol/day	7
Supersaturation Calcium Oxalate	10.11	Potassium, mmol/day	45
Calcium, mg/day	78	Magnesium, mg/day	52
Oxalate, mg/day	28	Phosphate, mg/day	0.76
Citrate, mg/day	11	NH4, mmol/day	68
Supersaturation Calcium Phosphate	0.71	Chloride, mmol/day	48
Urine pH	5.6	Sulphate, mEq/day	39
Supersaturation Uric Acid	2.71	Urea Nitrogen, g/day	11
Uric Acid, mg/day	0.499	Protein Catabolic Rate	1.2
Creatinine	1292

He has a high risk for calcium oxalate and uric acid stones. His urine citrate and sodium are remarkably low and he has a very low urine volume. His BP in the clinic was normal as were his labs apart from a serum creatinine of 1.3mg/dl

What is the underlying diagnosis (an important  piece has been left out of his background history)?
What is the best approach to treating his kidney stones?

Answers in the comments please (if this proves popular we may make it a regular feature).

Pearls for Boards

1) Surreptitious vomiting or diuretic abuse - metabolic alkalosis, Laxative abuse - non-gap metabolic acidosis.

2) Aquaporin 2 -  apical membrane of collecting duct, Aquaporins 3 and 4 - basolateral membrane of collecting duct, Aquaporin 1 - proximal tubule.

3)  Hemodialysis access rule of 6s: 6 weeks after the AV fistula has been placed, the fistula should:
1) be able to support a blood flow of 600 ml/min 2) be at a maximum of 6mm from the surface 3) have a diameter greater than 6mm.

4) Chronic lead exposure: 1) Interstitial nephritis 2) Gout 3) HTN

5) Calcineurin inhibitors, key differences - Tacrolimus: hair loss and higher rates of NODAT. Cyclosporin: hair growth and gum hyperplasia.

Pearls for Boards

1) In diabetic glomerular disease you can see linear staining of GBMs with IgG, Kappa and Lambda.

2) The three C3 immunoflourescence patterns of post strep GN 1) Starry Sky (most common) 2) Garland (less common) 3) Mesangial (resolving Starry Sky).

3) Troubles from Star Fruit 1) Seizures in dialysis patients 2) Hyperoxaluria -> AKI, Nephrocalcinosis, and Calcium Oxalate stones.

4) Avoiding aminoglycoside toxicity - reduce the dose frequency.

5) Membranous risk categories by proteinuria and renal function: Low - less than 4 g/day, normal fxn, Med - 4-8g/day normal fxn, High - more than 8g/day, abnormal fxn.

Pearls for Boards

1) Icodextrin sometimes causes a desquamating rash on the palms and soles.

2) Sirolimus, five side effects to watch 1) Poor wound healing 2) Lung toxicity 3) Hyperlipidemia 4) Proteinuria 5) Anemia/Thrombocytopenia.

3) Classic EM finding in post infectious GN: Large subepithelial hump shaped deposits.

4) Conivaptan is both a V2 and V1a antagonist - as such, contraindicated in cirrhosis were V1a agonists are used for variceal bleeding.

5) Eosinophilic peritonitis is not uncommon when breaking in a new PD catheter.

Pearls for Boards

1) Monoclonal Immunoglobulin Deposition Disease breakdown - 80 to 90% LCDD, 10 to 20% LHCDD, <5% HCDD.

2) Small studies suggest tamoxifen and steroids may be of benefit in management of Encapsulating Peritoneal Sclerosis in patients on PD.

3) Sodium restriction helps lower the risk of calcium nephrolithiasis by increasing proximal tubular uptake of sodium and subsequently calcium.

4) The age at presentation of anti-GBM disease has a bimodal distribution with a male predominance in younger patients and a female predominance in older patients.  More severe disease with lung involvement is more common in young patients while isolated GN is more common in older patients.

5) Hypothermia leads to potassium shift into cells and serum hypokalemia.

Pearls for Boards

1) Alkaline urine encourages calcium phosphate nephrolithiasis. Three predisposing factors to watch for - 1) distal RTAs 2) Acetazolamide 3) Topiramate.

2) IgA nephropathy, common in Asians and Native Americans, rare in African Americans.

3) Stay alert for triphasic pattern of water disturbance post neurosurgery or cerebral trauma - hypernatremia, hyponatremia and finally hypernatremia.

4) Long term PPI use can result in hypomagnesemia, hypocalcemia and hypokalemia.

5) Renal Malignancy Syndromes: Tuberous sclerosis - Angiomyolipomas and rarely RCC, Von Hippel Lindau - RCC and Pheo, Birt Hogg Dube Syndrome - chromophobe RCC.

Pearls for Boards

1) Topiramate - Watch for non-gap acidosis, nephrolithiasis and hyperammonemia.

2) Jak2 - the intracellular kinase activated by the binding of Epo to the Epo receptor.

3) Live vaccines are contraindicated in kidney transplant recipients – these include MMR, Varicella, Yellow fever and BCG.

4) Liddle's, the opposite of Pseudohypoaldosteronism Type I - Gitelman's, the opposite of Pseudohypoaldosteronism Type II (also known as Gordon's syndrome).

5) Myeloma cast nephropathy - distal intratubular casts, Light Chain Fanconi Syndrome - proximal intracellular crystals.

Pearls for Boards

1) Isopropyl alcohol does NOT cause an elevated anion gap acidosis, retinal toxicity (as does methanol), or renal failure (as does ethylene glycol).

2) Fibril diameter of the more common fibrillary diseases - Amyloid, Fibrillary GN, and Immunotactoid GP - is correlated with their position in the alphabet - (A= 8-12nm, F= 16-24nm, I= >30nm).

3) Drug induced ANCA disease - 3 to watch - propylthiouracil, hydralazine and minocycline.

4) The classic EM finding in Hereditary Nephritis is longitudinal splitting of the lamina densa of the GBM producing a laminated or "basket weave" appearance.

5) In individuals 40 years of age or older with a positive family history of ADPKD, a finding of zero or one renal cysts excludes the disease with a negative predictive value of 100%.

Nephrology Boards Study Strategy Post-Mortem

So after many months and a few intensive weeks of study the nephrology boards are now in the record books and I thought I'd examine what worked and didn't work in my study efforts.  If you're part of the board police, not to worry, no board content specific information will be shared here.

I started by taking a look at what Matt had previously written, including our own reader poll results about studying for the boards here on RFN.  Armed with this I, along with a couple other fellows, decided to use ASN board review course lecture notes, videos and questions as our core material.

We used the 2011 materials, I would have liked to have attended the live course but unfortunately was unable (and as Matt mentions, the all in cost of travel, hotel and course is high).  What I quickly re-learned as I watched the lecture videos (and I should have remembered from med school) is that I'm terrible at retaining things presented in lecture format.  While my colleagues were happily jotting down notes and remembering things, I was dozing off and wasting hours, having to re-visit what the heck was going on.

I switched over to a more active strategy of doing questions.  I used the questions available from the ASN board review course, NephSap (which has a huge bank of questions and answers) and those available through The Kidney Doctor.  I would do a question and then review each answer choice using UpToDate and my trusty Mass Gen Pocket Medicine 3rd edition from residency (which I was shocked to learn is now on it's 4th edition! I still have a battered and abused blue 1st edition from med school :).

I periodically joined up with my co-fellows using Google Hangout (which is free) to discuss broad sections of the ASN board review and practice questions.  Being interactive with others helped as it challenged me to be able to explain and articulate things which sometimes I wasn't crystal clear on and I picked up details that others had recognized and I had missed.

I occasionally dipped into Clinical Physiology of Acid-Base and Electrolyte Disorders by Rose and Treatment of Primary GN by Ponticelli and Glassock but for the most part I stuck with UpToDate due to the speed and ease of finding things.

Matt mentions he was disappointed with NephSap questions but I actually thought they were pretty good, particularly older versions and the Core Knowledge questions.  As board content experiences a lag between emergence in the literature and making it to the test, the past year or so of stuff generally isn't represented while stuff from a year or two before is starting to make it in.  The Pathology NephSap is particularly good and I would say a must review for path images.

The test is a now a bit longer for first time test takers than Matt mentions and now consists of four 60 question blocks.  I took a break after each section to clear my head and use the restroom and also took a break for lunch after the first two sections.  It's a long day, so pacing is key.

A final note (and shameless piece of self and RFN team promotion) is that RFN is a great resource!  Our new and archived content are a wealth of board review pearls and resources.  Best of luck in your own board review efforts and for those who have taken the test, let us know in the comments what worked and didn't work for you.

Board question: Hypertension-1 answer

The best answer is D.

Lifton et al. described a single gene mutation on the hormone-binding domain of the mineralocorticoid receptor (MCR). Individuals with this missense mutation develop early-onset hypertension with characteristic low renin and aldosterone levels. The mutation causes the MCR to be constitutively active, regardless of aldosterone levels, and transforms the MCR so that steroid hormones that are typically antagonistic become agonistic (in particular, progesterone and cortisone).

During pregnancy, when progesterone levels increase 100-fold, the MCR becomes hyperactive and leads to sodium reabsorption and potassium secretion via the principal cell of the distal collecting tubule (Figure above). The avid sodium retention and volume expansion appropriately suppress renin and aldosterone levels. This condition is not associated with proteinuria, edema, or neurologic changes, which distinguishes it from pre-eclampsia.

Given the low levels of aldosterone, this condition is refractory to standard medical therapy aimed at reducing aldosterone levels through RAAS blockade. In fact, mineralocorticoid receptor antagonists can actually exacerbate hypertension in this condition! Delivery of the fetus may be necessary to treat severe, refractory hypertension during pregnancy.

Essential hypertension results from a complex interplay of both genetic and environmental influences. Uncommonly, an isolated genetic mutation can engender hypertension, like in this case. These monogenic forms of hypertension affect either electrolyte transport in the distal nephron, or the synthesis and/or activity of mineralocorticoids, leading to a common final pathway of increased distal tubular reabsorption of sodium and chloride, volume expansion, and hypertension.

Other low renin, monogenic forms of hypertension include:

• Familial Hyperaldosteronism Type 1 (aka, glucocorticoid-remediable aldosteronism)
• Familial Hyperaldosteronism Type II
• Syndrome of apparent mineralocorticoid excess
• Liddle syndrome
• Pseudohypoaldosteronism type II (aka, Gordon syndrome)
• Congenital Adrenal Hyperplasia

They provide excellent fodder for any number of board-style questions!

Michael Lattanzio DO

Nephrology board prep

The results are in. Looks like the best way to study for the nephrology board exam, scheduled to be given on November 4th, 2010, is the ASN Board Review Course. I personally did not attend this course last year, but I did hear very good things about it. Comments from a course attendee- "it was focused, organized and worth the money". By no means is this course cheap. For fellows-in-training it cost $975 to register for the week long course (held August 28th-September 3rd, 2010). Not to mention the plane ticket to San Francisco and "special" hotel rate of $234 a day. Adding in miscellaneous costs (food, taxi etc) and this trip could cost you well over $2800. Add this to the outrageous fee of $2060 to take the nephrology boards and you can see why you don't want to take this test twice. So, for anyone interested, prepare to shell out $2,800.

• You can access all of the old powerpoint presentations on the ASN website for free.
  
• Buy the MP3 audio files of the entire conference for $147 or CD-ROM for $759.
• The ASN Board Review Syllabus is $450.
• Online ASN Board Review Course is $850.
  

Maybe some of the fellows or attendings can chime in on what they think about the ASN review course.

Next, in second place is the Brigham Renal Board Review Course (combined DVD and in-person). This is a 5 day course held in Boston, MA, August 9-13, 2010. Tuition is $695 and the Hotel rate is 119/night. I've also heard great things about this course. Personally, I did not attend this course, but instead purchased the DVD. Total Cost of Course- $2,000. The DVD's can be purchased for $1500. I found these useful especially the acid base and fluid/electrolyte sections.

Coming in third is Comprehensive Clinical Nephrology. Pictured to the left is the cover of the much awaited 4th edition taken from the Elsevier website scheduled to be released in September of 2010. My study group (consisting of 4 fellows) used the 3rd edition to prepare for last years exam. We started going through the text a few weeks after the in-service exam results were released (in early June) and finished in late September. The group met once every two weeks. We would each summarize 2-3 chapters at the bi-weekly meeting. So, we would go through about 8-10 chapters every 2 weeks allowing us to finish the entire book in 10 or so meetings (101 chapters). Overall, I think this method is difficult to achieve by oneself as the book is rather cumbersome. It really takes a group approach to get through this. Bottom line, this is a great textbook and something every fellow should have. I would only try using this book for board prep if you have a dedicated group.
Cost- $200.

Coming in at a tie for fourth is Renal Fellow Network and NephSAP. The RFN site and other popular nephrology specific websites (Uremic Frost, Nephron Power, Precious Bodily Fluids, Nephrology On Demand) have become an increasingly popular way to get relevant and easily digestible information. RFN has over 600 topics currently cataloged. I used renal fellow network extensively and thought it was a great way to read about interesting topics. We hope to continue this for years to come. Cost- Free

NephSAP was probably the most disappointing series from a board prep perspective in my view. To me, NephSAP is very detail oriented with much of the focus is on "cutting edge" research. The text was not helpful, in my opinion, for high yield study prep. However, you can access the online version of the exam questions which are worth reading a few weeks prior to the exam.

Cost- Free for fellows with the complimentary fellow ASN membership

Lastly, I included a few other options like UpToDate, The NKF Primer on Kidney Disease, Burton Rose- Acid Base and Journal Review Articles. Each of these can be useful study tools. Nate has already commented on the utility of Burton Rose-Acid Base which I would completely agree with. Interestingly, it seems that many institutions are forgoing their subscription to UpToDate secondary to cost. To purchase this on your own it will cost $195 for a trainee and $495 for a non-trainee (1-year). The Primer might be a better way to study as it is more concise than Comprehensive Clinical Nephrology. Maybe someone can comment on this.

In conclusion, I was a little disappointed with the study prep options available for the nephrology ABIM subspecialty exam. Especially with the multitude of options available for the Internal Medicine exam. My main problem was the lack of good question banks that are specifically geared for Nephrology. NephSAP provides a few, but this was hardly enough. The MKSAP nephrology section questions are a little to broad and frankly do not go into enough detail that a nephrology fellow needs. This is not, by any means, a comprehensive list of study options. I welcome any other options that I didn't include. A quick google search on this topic yields very little information. Good luck to anyone studying for the exam. My best piece of advice, "devise a plan early and stick to it".