Explanations for the 2014-2015 Official Step 2 CK Practice Questions

Update 8/5/2015:  They’ve now updated to the new 2015-16 question set and removed the old links (they’ve previously kept the old ones working for several years). You can still access cached versions of 2014-15 and 2013-14 for now (cachedview.com is helpful in cases like these). My explanations for the new set are available here.

Here are the explanations for the updated 2014 (effectively 2014-15) official “USMLE Step 2 CK Sample Test Questions,” which can be found here.

Overall, there are only three new questions when compared with last year’s set (#90, 95, and 104), which I’ve marked with asterisks below. The explanations for the earlier 2014 set (effectively 2013-14) set can still be found here (the question pdf is still available online) and are largely identical (though in completely different order).

Block 1

  7. F – Premature babies get neonatal respiratory distress syndrome due to surfactant deficiency.
  10. D – A boot-shaped heart means Tetrology of Fallot on board exams. Outside of that giveaway, TOF is by far the most common cause of cyanotic heart disease.
  23. B – You can usually ignore the CT scan if you want. Elevated lipase, epigastric pain radiating to the back, and alcoholism go best with pancreatitis. Varices present with hematemesis. Perforated gastric ulcers will give you free air (also typically blood in the stool as well).

Block 2

  31. B – Diabetes get diabetic nephropathy. Don’t over-think things.
  43. E – This question is comical. They even included the munchies.
  44. B – Urinary symptoms (dysuria, urgency, frequency)  and positive urinalysis (leukocyte esterase and/or nitrite) without flank pain or systemic signs (fever, rigors, malaise, elevated white count) means simple acute cystitis. Add the other things, you get pyelonephritis.

Block 3

  3. D –The radiograph is showing complete collapse of the left lung (2/2 mucous plugging) with resultant severe mediastinal shift. Acute shift of this acutely can have the same effect as any other “tension”-type process, causing impaired venous return to the heart and decreased cardiac output via the Starling mechanism.
  6. C – Increasing pain after injury and casting, particularly with passive motion, means compartment syndrome. Compartment syndrome treatmentseems is barbaric, but a fasciotomy prevents neurovascular compromise.
  8. D – Atopic dermatitis (eczema) is the “itch that rashes.” It’s one leg of theallergic triad: asthma, allergic rhinitis, and atopic dermatitis. Treatment is with topical steroids and rigorous emollient therapy.
  9. B – This patient has chronic (6 weeks) symptomatic hypotension while not coincidentally on three BP meds: a dieuretic, a beta blocker, and an ACE inhibitor. The most likely explanation and easiest/fastest intervention is to reduce her polypharmacy.*
  11. A – Lisinopril and especially spironolactone (a K-sparing diuretic) both cause hyperkalemia. Renal failure (severe AKI or ESRD) is also a major cause of hyperkalemia, but not with the only mildly elevated Cr and BUN levels.
  14. A – Proximal muscle weakness with skin findings means dermatomyositis.
  30. B – Acutely increased sputum production in a patient with COPD equals an exacerbation, which can be treated with steroid and antibiotics. The big-time smoking history automatically implies the COPD diagnosis; the ipratropium prescription cinches it.



  1. 1) Most importantly, he has a high grade fever, which implies aspiration pneumonia (infection) over chemical pneumonitis (sterile).
    2) Chemical pneumonitis on a test would is more likely to refer to someone huffing gasoline than puke.

  2. Thank you for this! Love your site! A quick comment for #50:

    50) Infertility in males with cystic fibrosis is due to bilateral absence of the vas deferens. They are infertile, not sterile, and a sperm sample can be taken directly from the epididymis and used in assisted reproduction. For women with CF, 20% will be infertile, secondary to thick cervical mucus which blocks sperm entry.

  3. For question 85, the correct answer is acute cystitis; in your explanation you note a positive urinalysis points to this diagnosis — leukocyte esterase and nitrite — but the patient actually had NO nitrites. I think everything else points toward acute cystitis so it didn’t really matter that there were no nitrites. At least, that was my thinking.

  4. It’s supposed to read “and/or,” thanks for the catch. The UA for this patient is still definitely positive. Leukocyte esterase is a WBC enzyme produced by the patient, whereas nitrites are only produced by some urinary pathogens, particularly E. coli.

  5. Yet another awesome post — huge thanks for this. Quick question though: On Q #95, the question describes carotid U/S findings of reverse flow without occlusion. I presumed this to be subclavian steal syndrome when coupled with the BP difference in her arms, only to find my thinking apparently way off base. What are these findings indicative of?

  6. Your thought was largely correct. One thing to keep in mind is that subclavian steal is a supply/demand phenomenon and not a constant process. In many patients, subclavian steal can be asymptomatic. In this patient’s case, she is truly orthostatic (dizzy when stands up with a drop of 40 mmHg systolic!) and also has sinus bradycardia. So she has tenuous cerebral perfusion at baseline and is ripe for symptomatic steal as well. Treating her polypharmacy can fix her orthostasis and may even fix her steal (With better resting blood pressure and supply to the arm, the steal may not even occur).

  7. Sorry, I haven’t gotten around to doing those (in part because my main computer is a Mac and can’t run the software).

  8. Hi Thanx for the explanations
    About q 125- The clinical findings is consistent with asthma but spirometry findings are not…it’s supposed that FEV1 SHOULD BE DECREASED AND FEV1/FVC TOO .. ????? That;s why i did not ANSWER asthma ..

  9. Quick question regarding practice test vs software… are the questions the same between the PDF and the software? I have a mac, and can’t access the software.

  10. PDF and software questions are the same with the exception that the software also includes a few multimedia questions.

  11. hey, the pdf documents for the 2013-2014 and 2014-2015 practice papers no longer work. does anyone have another way I could access these? many thanks

  12. Looks like they’ve just updated to the new question set and removed the old links (they used to keep the old ones working for several years back). You can still access Google cache versions of 2014-15 and 2013-14 for now (cachedview.com is helpful in cases like these). At some point when I have some time I’ll tackle the new set; typically many if not most questions overlap year to year.

  13. First of all, this is super helpful so thank you! Second, I am still having a hard time with 97. I kept going back and forth between A and D. In your explanation you state that A is more likely given the normal BUN. But 40 isn’t normal. So can you explain more how you chose A? In my mind (which is probably wrong), a patient with hypertension is set up for renal failure, and the renal failure would then lead to problems with medications. So it was kind of a chicken vs. egg question for me.

  14. Cr 1.8 and BUN of 40 are both mildly elevated but not egregious. In order to have massive potententially fatal hyperkalemia, you’d 100% need to look for additional causes. In his case, we aren’t even told his baseline, so we don’t technically know if he’s in AKI or simply has CRF (but BUN:Cr ratio > 2:1 suggests a dehydration/prerenal state). When patients with ESRD have hyperkalemia secondary to renal failure, their BUNs will typically be way higher (i.e. 75, often greater than 100).

    HTN of his level certainly can lead to some degree of chronic renal failure. For his current acute condition, it’s more likely, given the history of nausea and BUN:Cr ratio, that his PO intake is low (or that he also has emesis), and he is volume depleted. Volume depletion potentiates hyperkalemia in those on K-sparing diuretics and ACE-inhibitors and is also by far the most common cause of AKI. Malignant hypertension can cause AKI as well, but not 140/90.

    The short answer: people with Cr of 1.8 (even acutely) generally don’t spontaneously develop a potassium of 7. So while renal failure certainly exacerbates the expected medications effects, the proximate cause is still the meds. The renal failure itself wouldn’t cause his problem.

  15. Question:
    22 y/o who got shot. Vitals:
    Answer: thoracostomy
    Why would you not intubate first?
    When do you answer intubation on the test?

  16. My guess was because his “airway” is in general protected, his issue is “breathing” i.e. lung is filled with something. He needs this corrected before he can get stabilized and securing an airway won’t do that. Now, if his airway wasn’t secure (no sounds on either side due to poor passage of air) you’d have to intubate first, but he’s getting air in — it just can’t diffuse because his alveoli are clogged with something. From medscape: “Tube thoracostomy is the insertion of a tube (chest tube) into the pleural cavity to drain air, blood, bile, pus, or other fluids.[5] Whether the accumulation of air or fluid is the result of rapid traumatic filling with air or blood or an insidious malignant exudative fluid, placement of a chest tube allows for continuous, large volume drainage until the underlying pathology can be more formally addressed.”

    Response to
    22 y/o who got shot. Vitals:
    Answer: thoracostomy
    Why would you not intubate first?
    When do you answer intubation on the test?”

  17. BB’s explanation is correct. In the ABCs, his issue is with B and not A. The question isn’t whether he will get intubated, the issue is nearly always what happens first.

    Intubation will be the answer on the test in several scenarios but primarily in situations in which the patient’s mental status results in the inability to safely maintain the airway or direct involvement (e.g. swelling) results in mechanical airway compromise. Examples would include head trauma with GCS suppression, severe alcohol or drug intoxication, and mechanical issues from infection (epiglottitis), allergies (laryngeal edema), or facial/neck trauma.

  18. For #50, I thought it was CF, but why is his presentation so late? No mention of him not being born in US (and therefore screened) and the infxns have been only happening for 4 yrs? Really threw me off.

  19. Depends on the mutation you have, what sort of residual activity you have, and consequently how severe your disease is. Even carriers can have significant symptoms, though conventional wisdom is that they should be asymptomatic as CF is AR. Mild disease can present in teen years or adulthood. Severe disease may not survive childhood.

    Newborn screening for CF is done by blood test, which is less sensitive than the sweat test for CF, particularly so in mild disease (it measures a pancreatic enzyme).

    And lastly, perhaps most importantly, newborn CF screening is recent. It started in the 1990s and didn’t hit all 50 states until 2010. Therefore there are a lot of kids alive who haven’t been screened, particularly teenagers. These timing issues are occasionally important for Step (e.g. when blood transfusions screening began for HIV and HCV to determine potential prior exposure or when varicella vaccine became commonplace because adults of a certain age may not be immune if they didn’t have it as kids.)

  20. hi,
    I got 26 wrong question wrong q’s, and I would like to know the correlation of it. Don’t know what happened with the system it did not show any % at the end of the test. If you can help me I’ll appreciate

    thank you.

    • Impossible to say for sure. I don’t remember the total length including multimedia questions, but 26 wrong out of 131 would correspond to 80%, which is probably around 220.


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