Here are my explanations for the new NBME 2018 USMLE Step 1 Sample Test Questions. This year there are 51 new ones (marked with asterisks).
Like in years past, the question order here is for the PDF version (not the FRED-simulated browser version). This facilitates using these explanations in future years when they change the available question set (because the old ones are always available via archive.org). The multimedia explanations are at the end.
Prior sets/explanations can be found here.
- D – Schistosomiasis is a parasitic worm particularly endemic in Africa (Egypt, in particular, comes up the most on questions) that is most associated with chronic cystitis. Calcifications of the bladder wall are essentially pathognomonic. Chronic infection is associated with an increased risk of squamous cell carcinoma of the bladder (as opposed to the usual urothelial/transitional cell).
- A – Basic nerve anatomy and function.*
- D – Hot tub folliculitis, it’s a thing. Classically pseudomonas.*
- A – Acting out aka “being a teenager.”*
- E – VEGF is a major tissue growth factor activated by injury, cytokine release (infection, inflammation) and hypoxia that promotes angiogenesis and also increases vascular permeability (hence the edema). This increased permeability aids in the movement of proteins and white blood cells to the site of injury.
- C – Pseudogout is caused by positively-birefringent rhomboid calcium pyrophosphate crystal deposition. Most commonly affected location is the knee. Contrast with gout, negatively birefringent, big toe. A differential for both to keep in mind is septic arthritis.*
- C – Filgrastim is a granulocyte colony stimulating factor (GCSF), which are drugs used to increase white blood cell count in patients with leukopenia. Leucovorin (folinic acid) sounds like it would also be right, but it’s used to prevent bone marrow suppression in patients taking methotrexate. Darbepoetin (like erythropoietin) is used to stimulate red blood cell production.
- B – The left-sided system is much higher pressure than the right side, hence the aortic valve closing is usually louder than the pulmonic valve. A P2 louder than A2 means that the pulmonary arterial pressure is significantly elevated.
- C – Southern blots are commonly used in immunological studies, as the southern blot allows for the study of DNA alterations. What is normally one gene configuration related to immune globulins in most tissues demonstrates multiple different bands in the bone marrow, indicative of gene rearrangement. This is basically how we create new antibodies. Reactive processes are polyclonal (multiple bands); leukemia, in contrast, is monoclonal (single band).*
- F – Total peripheral resistance goes down during exercise as the arterioles supplying muscle and skin dilate.*
- D – The baroreceptors are stretch receptors (the more fluid in the vessel, the more they fire). So a patient with hemorrhagic shock will see a decrease in the baroreceptor firing rate. Activation of RAAS will result in increased vascular resistance (vasoconstriction) in order to maintain blood pressure. And capillaries, such as those in the kidney, will be primed for resorption and not filtration (no one wants to pee out good dilute urine when they’re dehydrated). Likewise, systemic capillaries will prefer to hold onto plasma and not let it leak into the interstitium (third-spacing).
- E – PCP is a sedative-hypnotic and dissociative anesthetic that generally acts as a downer but can also cause incredible aggression coupled with pain insensitivity (the superman drug). Vertical nystagmus is a commonly mentioned physical exam finding.
- C – The Pouch of Douglas is the space between the uterus and the rectum (i.e. the place where pelvic free fluid goes).
- D – The “migratory serpiginous perianal rash” (ick) is classic for strongyloides, a parasitic roundworm acquired from larvae-contaminated soil. Strongyloides larvae can borrow (hence the rash) and can migrate to the GI tract and lay their eggs, which then hatch in the intestine and cause diarrhea. Treatment is Ivermectin (and if not, mebendazole/albendazole). Checking the stools for larvae is the most sensitive test. Parasite life cycles are gross.
- C – Leydig cells make testosterone. Leydig cell tumors aren’t always physiologically active, but those that are can cause masculinization. Granulosa cell tumors, on the other hand, sometimes produce estrogen (which can lead to precocious puberty in young girls but otherwise may be occult). Teratomas are oddballs that typically have fat, hair, teeth, etc. Thecomas will not be on your test. Ovarian carcinoid is highly unlikely to show up on your test, but if it did, it would likely present with a classic carcinoid syndrome.
- A – Pulmonary fibrosis (a restrictive pattern disease) is a major cause of mortality for patients with scleroderma. Logically, if the disease causes fibrosis elsewhere, it’s going to cause fibrosis in the lungs.
- D – Sensitivity rules things out. It’s TP / (TP + FN). So in order to calculate the sensitivity of this test, we need the true positives (the 90 with cancer) and the false negatives: the patients for whom the test is negative but actually do have prostate cancer. That’s D.
- B – Bisphosphonates work by decreasing osteoclast activity (thereby reducing bone resorption). Choice F is the opposite of how estrogen therapy works (RANKL is found on osteoblasts, and its activation triggers osteoclasts and stimulates bone resorption).
- B – Memorize aspirin’s unique acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is likely actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.
- B – Note that the question is not asking what cells fight URIs. The question asks what lab finding would be consistent with decreased immune activity (and thus the only choice that matches “decreased” with an immune cell is the best answer).
- B – Don’t let them blind you with this patient’s misery. The issue of the day is that he has a DVT. That’s why he came to the ER in the first sentence and what the ultrasound shows at the end. Patients with cancer are hypercoagulable.*
- E – Endothelial tight junctions’ permeability is increased in response to injury and inflammation, allowing migration of white blood cells and friends to the site of injury.
- A – Endemic Burkitt lymphoma can happen in Brazil as well as Africa (jaw lesion, puffy face). The photomicrograph is demonstrating tingible body macrophages, a type of macrophage containing many phagocytized, apoptotic cells in various states of degradation.
- A – p53 is the quintessential tumor suppressor (it activates apoptosis). HPV carcinogenesis is caused by insertion of the virus into host DNA that produces a protein which binds to an essential p53 substrate, functionally inactivating p53 and preventing its apoptotic cascade. C (transactivation/TAX) is how HIV and HTLV cause cancer. E (c-myc translocation) causes Burkitt lymphoma.
- A – DI is an important complication of some skull base fractures and can be treated with DDAVP. You probably remember that this works via the activation of aquaporin channels, but these are moved from intracellular vesicles to the apical membrane surface as a result of a DDAVP-mediated increase adenylate cyclase via a stimulatory G protein that increases intracellular cAMP.*
- B – Crohn’s: skip lesions, fistulae, strictures (and the unnecessary transmural involvement on histology).
- C – The mom will pass on her deletion in 50%. The father will pass it on in 100% (because both of his copies are affected). Therefore, the child will automatically have at least one deletion and will have the double deletion in 50%.*
- C – Approximate fasting physiology timing: the post-absorptive phase (6-24 hours after a meal) is dominated by glycogenolysis. Gluconeogenesis from 24 hours to 2 days. Then ketosis.*
- B – The arrow is pointing to a neutrophil (multilobed nucleus): main fighter of the immune system in acute inflammation and bacterial infection (such as aspiration pneumonia). C5a is a chemotactic factor for PMNs.
- C – While E coli is normal gut flora, your body would prefer it stay intraluminal.*
- A – Air and fluid = hydropneumothorax. If that fluid is blood (s/p stabbing), it’s a hemopneumothorax. Lack of mediastinal shift indicates that it’s not under tension.
- E – von Willebrand disease is by far the most common inherited bleeding diathesis. Frequently, the only laboratory abnormality is increased bleeding time (literally you prick the patient and see how long it takes them to stop bleeding). On Step, bleeding women have VWD. Bleeding boys have hemophilia.
- E – Fragile X is a CGG trinucleotide repeat expansion disorder (which like Huntington’s is a test favorite). The maternal uncle is the hint to the X-linked inheritance. Autism-like behaviors and relatively large head are common; large testicles only appear after puberty.
- E – Gram-positive rods in a diabetic foot wound (or a World War I soldier fighting in a trench) means Clostridium perfringens (the causative organism of gas gangrene). Crepitus means gas in the tissues, which is produced as a byproduct of its highly virulent alpha toxin.
- D – He has (presumably RSV) bronchiolitis. RSV is an RNA virus that enters the cell via a fusion protein (which is the target of the prophylactic monoclonal antibody drug Palivizumab).*
- D – A b2 agonist like the bronchodilator albuterol would sure help that wheezing. Note that epinephrine (such as in an epi-pen) would also achieve this but is nonselective; in this case, the patient’s symptoms would be helped most by the beta-2 component.*
- C – The purpose of Rhogam is to bind to and remove the RhD antigens so that the mother does not form an immune response against the antigen in fetus’ blood. It’s given to at-risk Rh- moms at 28 weeks and at delivery.*
- C – Metformin is awesome. It decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.*
- A – Gonorrhea can change its pilus, which is responsible for adhesion to host cells and the main antigen to which the host mounts an immune response. Neisseria gonorrhoeae is able to switch out different pilin genes, and for this reason, prior infection does not confer long-lasting immunity.
- B – Anorexia leads to hypogonadotropic hypogonadism, as the body realizes that the possibility of nourishing a fetus is zero and gives up the pretense. There’s a lot of supporting data, but one should guess this answer once you read the word “gymnast” (or “dancer”).
- C – Statins raise HDL and decrease LDL and TGs. Their effect on LDL is by far the most potent, but they do a little good on everything.
- E – Androgens stimulate sebaceous glands and cause acne. In girls, this is primarily due to adrenarche (DHEA/DHEAS androgen production made by the adrenal gland the zona reticularis). Boys can also blame testosterone from gonadal puberty (pubarche).
- D –Diffuse low-level ST elevation means pericarditis. These patients often complain of pleuritic chest pain that is somewhat alleviated by sitting up and leaning forward and have distant heart sounds. Common test causes include viruses, uremia, and 2-3 weeks after myocardial infarction (Dressler syndrome).
- A – Electrical alternans on boards means a big pericardial effusion (and usually cardiac tamponade physiology). The heart cannot fill properly, preload decreases, hypotension and tachycardia ensue, fluid backup leads to elevated JVP. Underlying etiology in this patient is renal failure.
- B – Codeine is a prodrug with basically no analgesic effects by itself. It instead must be metabolized (mostly by the liver via CYP2D6) into morphine in order to provide analgesia. Some folks convert more, some less.*
- A – Ah, countertransference. Remember that transference is when the patient is transferring (redirecting) feelings about someone on to you (you remind them of their dad). Countertransference is when you do it about them (they remind you of your son). Projection is when you assign your own feelings to them (you are angry, so you think you they are angry).
- C – Serum sickness! A type III (immune complex) hypersensitivity.
- B – You will remember that G6PD deficiency causes red blood cells to break down in response to certain stressors, infections, and drugs. The patient’s symptoms are a manifestation of indirect hyperbilirubinemia due to hemolysis (RBC breakdown). Sulfa, fava beans, nitrofurantoin, isoniazid, and antimalarials (e.g. primaquine) are the common test favorites.* This question was also updated since the original PDF was released, as a helpful reader pointed out below. It is a now a case of bubonic plague (or possibly ulceroglandular Tularemia), both which are treated by answer choice E, which refers to aminoglycosides, which target the 30S ribosomal subunit. Please see the 2019 explanations.
- D – The effects of excess thyroid hormone: attempted compensatory TSH suppression, increase in both T4 and free T4, and normal TBG. Note that the question doesn’t even hinge on TBG and is also unlikely to on the real thing.
- D – Carbamazepine is a notorious CYP450 inducer, so you should be guessing metabolism no matter what. CYP450 plays an important role in both vitamin D bioactivation and degradation in the liver.*
- C – This is obviously a clinical trial. If you know you are getting a drug, then you are not blinded: it’s an open-label trial. There is no randomization as there is only a single treatment group.
- G –Vincristine (a mitosis inhibitor) frequently causes peripheral neuropathy, which can be severe and irreversible. Other fun associations are Bleomycin with pulmonary fibrosis, Cyclophosphamide and bladder cancer, and Doxorubicin with dilated cardiomyopathy.
- C – Acetylcholine increases after drug X, which is the same we’d expect if drug X were a cholinesterase inhibitor.*
- B – This question is a little bit BS, in that there is nothing in the stem at all to make you think this specifically. What the question is trying to ask is what factors cause malpractice suits in general. While professional competence is a cause, people love to discuss and the boards love to test about poor physician communication and lack of empathy as root causes.
- D – The scenario described is heart failure 2/2 mitral valve regurgitation. If we want to prove the regurg, we can confirm and grade it using an echo.*
- E – Pubertal gynecomastia in males is normal and generally goes away on its own. If “normal” is an answer choice, make really sure you don’t want to pick it.
- E – Multiple infections. Abscesses. Then you hear decreased oxidative burst and immediately think NADPH oxidase deficiency aka Chronic granulomatous disease, which causes recurrent abscess-forming infections due to the inability to kill ingested organisms because of the inability to generate superoxide radicals.*
- D – Relationship with former patients are generally frowned on, but they’re especially problematic if the patient was a psychiatric patient, as the power imbalance of the practitioner-patient relationship and information the provider is privy to because of their patient care involvement preclude a healthy balanced relationship of equals.
- E – Subacute combined degeneration (progressive peripheral sensory and motor loss) is a late sign of B12 deficiency, which is common in old people. On exams, a geriatric patient who lives alone and may have a “tea and toast” diet is likely to have vitamin deficiencies, particularly of folate and B12.
- A – The infraspinatus and teres minor are responsible for external rotation. Both the infraspinatus and supraspinatus muscles are innervated by a suprascapular nerve.
- A – Fear = amygdala*
- A – The alpha-value corresponds to the p-value we will accept as significant and reflects the likelihood of a type I error (a false positive). A lower alpha-value means a lower acceptable likelihood of obtaining the same results by chance, and thus, significant results can be reported more confidently (a 1% false positive rate instead of a 5% rate).
- C – Swallowing amniotic fluid is a critical component of lung development. Fetuses with severe oligohydramnios are plagued by pulmonary hypoplasia, which is the cause of death in fetuses born with Potter syndrome (renal agenesis).
- C – This question is asking for the vascular supply of the parathyroid glands. That would be the inferior thyroid arteries, which arise from the thyrocervical trunk.*
- B – Thiazides (typically used as antihypertensives) also increase calcium resorption in the distal tubule and are therefore useful in preventing calcium oxalate stone formation in patients with hypercalciuria (the mechanism is not really worth learning). Thiazides block the Na-Cl symporter, as opposed to loop diuretics, which block the triporter, and acetazolamide, which blocks carbonic anhydrase in the proximal tubule.
- A – A new blistering disease in an older person is typically going to be a pemphigus question. Then you just have to remember the difference between bullous pemphigoid vs pemphigus vulgaris. Bullous pemphigoid is characterized by the loss of hemidesmosomes that bind keratinocytes to the basement membrane, resulting in bulla (big blisters) in areas of friction, choice A. Patients with pemphigus vulgaris lose their desmosomes (which bind keratinocytes to each other), so that their skin is super friable, which results in ulceration. Mouth ulcers are more common in PV.
- B – The Lincoln’s beard distribution described is that of the V3 branch of the trigeminal nerve, which exits the skull base via foramen ovale. V2 exits via foramen rotundum. V1 exits via the superior orbital fissure.*
- E – Splitting is an immature defense mechanism often employed by patients with borderline personality disorder. When splitting, a person fails to see others as capable of having both positive and negative qualities; at any given time, it’s all or nothing.
- D – PMA activates NADPH-oxidase, such as seen in the oxidative burst. In this case, this stimulation produces no response, suggesting NADPH-oxidase deficiency (which means this is another question about chronic granulomatous disease). The organism should thus be an abscess forming bacteria such as staph aureus. Oh wait, that’s what the question described anyway (two-year-old with recurrent abscesses), meaning that the PMA nonsense was basically superfluous.* (If your answer key says E, then you’re looking at the 2019 set. See the explanation for the newer version of this question here).
- A – As always, it’s almost better to ignore the pictures when possible. This gentleman has a peptic ulcer, which we know is caused predominately by H. pylori infection. H. pylori produces proteases and particularly urease, which allow it to increase the pH of its local environment by cleaving urea into ammonia, which is toxic to gastric mucosa. The picture demonstrates H pylori, which are evident with silver staining.
- B – A genetic variation in a particular nucleotide is by definition a polymorphism. Note that the question specifically states that it does not change the protein.*
- C – TTP has a classic pentad: microangiopathic hemolytic anemia, thrombotic purpura, fever, renal failure, neurologic abnormalities (AMS). Whenever you see a question where the patient suddenly has a lot going on, consider TTP.*
- A – Androgen insensitivity is caused by a defective androgen receptor. DHT is responsible for creating male genitalia during fetal sexual development. The default human gender is female. So a genetically male patient with complete androgen insensitivity is externally phenotypically female. Lack of response to adrenal androgens prevents hair formation during puberty (adrenarche).
- A – Intermittent hyperbilirubinemia/jaundice in an otherwise healthy individual is typical of Gilbert’s syndrome, which is caused by the decreased activity of UDP glucuronosyltransferase.*
- A – An annular pancreas surrounds the duodenum and can cause intermittent duodenal obstruction. While this question theoretically requires the imaging to answer correctly, the only other choice that is feasible is D, which is known as SMA syndrome. SMA syndrome is quite rare and typically seen in people who have recently had significant weight loss. On the imaging, it would be smooshing of the duodenum by a bright contrast filled artery as opposed to surrounding by soft tissue. I also think it’s highly unlikely to be tested.*
- A – The usual cold-like symptoms of runny eyes and a sore throat are common of several strains of adenovirus that are readily communicated amongst humans in close contact.*
- D – The arrowed fluid is contained in a space behind the stomach but in front of the retroperitoneal structures (e.g. the pancreas), i.e. the lesser sac.
- B – This is a (prospective) case series. There is no control group (and certainly no blinding).
- E – Calcium oxalate stones are the most common variety of kidney stones, but uric acid stones make up 5-10% as well. None of the other choices are associated with renal calculi of any variety.
- E – The patient’s chronic inflammatory pneumonitis is killing off his lung parenchyma (composed primarily of type I pneumocytes). Type II pneumocytes, in addition to making surfactant, can replicate in order to replace type I pneumocytes, so they will be increased. Chronic interstitial inflammation results in fibrosis, hence an increase in fibroblasts.
- A – Malonyl-CoA inhibits the rate-limiting step in the beta-oxidation of fatty acid. Logically, resting muscle requires less energy (and thus less need for fatty acid breakdown) than active muscle.
- E – Timolol is a beta-blocker. Beta blockers can exacerbate asthma/COPD/reactive airway disease.*
- E – No relation between the atrium (P) waves and the QRS complex means third-degree AV block (aka “complete” heart block). Symptomatic (even fatal) bradycardia can result. “Cannon” a(trial) waves are prominent jugular venous pulsations that occur when the atria and ventricle contract simultaneously (which, of course, doesn’t normally happen).*
- E – CNS amoebiasis is most notoriously caused by Naegleria fowleri, which I encourage you to memorize as the “brain-eating amoeba.” Found in fresh-water bodies of water like ponds and lakes, it has three forms: a cyst, a trophozoite (ameboid), and a biflagellate (i.e. has two flagella). Infection is via olfactory cell axons through the cribriform plate to the brain.*
- E – Functional parathyroid adenomas can cause elevated parathyroid hormone (PTH), which results in hypercalcemia and hypophosphatemia. Hypercalcemia is characterized by the rhyming symptoms: stones (renal, biliary), bones (including bone pain to osteitis fibrosa cystica), groans (abdominal pain, n/v), thrones (polyuria, constipation), and psychiatric overtones (from depression to coma).
- A – The main downside of live vaccines is that they rarely cause the disease they’re designed to prevent, typically in immune-compromised individuals (who either get the vaccine or are close contact to someone who does)*.
- B – They have described what you assume is a classic case of pneumonia. But, PNA isn’t an answer choice. What the next best thing? The cause! Old frail people (and alcoholics) love to get aspiration pneumonia. RLL is the most common site, which they have provided (thank you, big vertical bronchus). They even gave you the hint that the patient has “difficulty swallowing,” which is code for “aspirates when swallowing.”*
- B – The proliferative phase of the menstrual cycle is controlled by cyclin-dependent kinases.*
- C – Stroke characterized by left hemiparesis and right CN12 palsy. Crossed findings mean a brainstem lesion. Right (ipsilateral) tongue, left-sided (contralateral) weakness means the exiting right hypoglossal nerve has been affected (within the right medulla). C is the pyramid where the corticospinal tract runs to control muscles (prior to the decussation). This is known as the medial medullary syndrome or Dejerine syndrome.
- E – This patient has chronic kidney disease, as indicated by elevated serum creatinine/BUN and evidence of anemia of chronic disease (normochromic normocytic). Poorly functioning kidneys do not hydroxylate 25-Dihydroxycholecalciferol to 1,25-Dihydroxycholecalciferol well nor produce adequate erythropoietin (hence the CKD-related anemia). Patient’s with CKD thus develop secondary hyperparathyroidism due to deranged phosphate excretion and inadequate Vitamin D activation resulting in hypocalcemia. Thus, we should expect to see low calcium, high phosphorus, low 1,25 vitamin D, and low Epo, which is E.
- C – There is an inferior orbital wall blow-out fracture. If you happen to know CT anatomy, this is actually involving the infraorbital foramen, which transmits the infraorbital artery and nerve, but really, so long as you notice the obvious fracture it’s the only choice that makes sense.*
- C – Stress-related bowel issues, sometimes but not always alternatively involving both diarrhea and constipation, are a hallmark of irritable bowel syndrome (IBS). A diagnosis of exclusion, most of the stem is helping you rule out more serious issues. Lubiprostone, which is a fatty acid that induces stool-softening intestinal secretions, is approved for idiopathic constipation, most commonly in the context of IBS and or secondary to opiate use. The other drugs listed are for IBD.*
- B – Blood at the meatus is the red flag (see what I did there?) for urethral injury, which should be evaluated for with a retrograde urethrogram. The membranous the most commonly injured by fracture. In contrast, the spongy urethra is most likely to be injured during traumatic catheter insertion or in a straddle injury.*
- A – Oral vesicle (hint hint). Blistering vesicular lesion on the hand. No fever, not toxic-appearing. This is Herpes (you may remember dentists getting herpetic whitlow in your studies, which is what this is). Most folks get HSV1 as children, though obviously not all are symptomatic. HSV is a large double-stranded, linear DNA virus.*
- F – Many autoimmune/autoinflammatory conditions, including ankylosing spondylitis, are treated with DMARDs like anti-TNF-alpha medications when milder stuff doesn’t do the trick. Common examples are infliximab (Remicade) and adalimumab (Humira).*
- D – If the fluid keeps coming into the glomerulus (via the afferent arteriole), but you clamp the exiting vessel (the efferent arteriole), then it’s going to build up in the glomerulus, leading to increased hydrostatic pressure.*
- D – SIADH is a test favorite a very common cause of hyponatremia (after dehydration). A variety of brain and lung pathologies are possible etiologies, with lung cancer (of any type) being an important cause.
- E – DMD is X-linked. We know her mom is a carrier based on family history, supported by lab testing. But her mom has 2 X chromosomes, only one of which is mutated. There is no way to know which her daughter eventually receives and expresses by her phenotype (i.e if she is a carrier or not). Just because her CK is normal doesn’t mean she isn’t a carrier–the phenotype of the X-linked carrier depends on X-inactivation.
- B – Absolute risk reduction is the decrease in the number affected per number exposed = (15-5)/50 = 10/50 = 0.2.*
- B – This requires no explanation.*
- B – What we have here is a congenital intolerance to breast milk: galactosemia, in which the body cannot convert galactose to glucose (resulting in an accumulation of Galactose 1-phosphate). They then list the findings and tests used to diagnose it. Lactose (the disaccharide in milk) is composed of glucose + galactose.
- C – Just because he’s having (unprotected) sex doesn’t mean he doesn’t have simple infectious mononucleosis. The sex implies he’s also kissing someone! Pharyngitis + lymph nodes + fatigue = mono.
- D – An odds ratio greater than 1 signifies increases odds/risk/likelihood. If the 95% confidence interval range does not include 1, then the difference is statistically significant (though not necessarily clinically meaningful).
- C – Osgood-Schlatter is also known as apophysitis of the tibial tubercle. It’s due to chronic stress/irritation at the insertion of the patellar tendon on the tibial tubercle. It’s classically seen in teenagers doing repetitive vigorous activity (running, jumping). The radiograph demonstrates classic fragmentation of the tibial tubercle (which isn’t necessary to recognize to get the question correct).
- B – BK virus reactivation is a cause of renal damage post-transplant in the setting of immune suppression, also known as BK nephropathy. Treatment is a reduction in immune suppression, allowing the body a chance to fight back. The virus can cause a cold-like URI syndrome with fever.*
- E – Specificity is the ability to accurately predict true negatives: TN / (TN + FP) = 95 / (95+5) = 95%*
- E – Cystic fibrosis is an autosomal recessive disease involving CFTR, which means you need a double hit to express the disease. If the genetic test only picked up one, then it must have missed the other.*
- B – (Unstable) angina. Most immediate treatment is nitro.*
- B – To amplify tiny fragments of DNA in order to detect their presence, we use PCR. The question is a description of the process. Southern Blots are used to detect a specific DNA sequence within a DNA sample.
- A – Targetoid rash after a woodland excursion means Lyme disease, caused by Borrelia burgdorferi, carried by the Ixodes tick. Rash (erythema migrans), viral syndrome symptoms, fatigue, and polyarthritis are common. Lyme carditis typically manifests as AV block.
- A – Narcotic use for acutely painful conditions is both reasonable and important. (Very) short-term use (immediately post-surgical) does not lead to long-term dependence (or so people have thought…). And yes, drugs addicts should also receive narcotics to control pain.
- D – Many oral cavity lesions, especially anteriorly such as the tip of the tongue, drain first to submental nodes (level 1). Oropharyngeal SCCs most commonly drain to level 2.*
- C – This patient has hepatitis (elevated liver enzymes) due to active Hepatitis C infection. Hep C and HIV infection are both associated with intravenous drug use. While most patients with Hep A will clear the virus after their acute illness, Hep C causes chronic infection in 80% of patients, which may lead to cirrhosis over time (~20 years).
- B – p53 is an important tumor suppressor gene, particularly in its ability to cause a cell to undergo apoptosis in the event of damage. p53 activity also holds the cell at the G1/S regulation point (B), limiting DNA synthesis.
- D – The only thing that directly raises BP of the list is increased PVR.*
- D – Below the dentate line, anal cancer drainage is superficial inguinal. Above the dentate line, superior rectal (then iliac).*
- C – A history of volume loss (often GI 2/2 vomiting, diarrhea) resulting in shock is consistent with a hypovolemic etiology, as corroborated by the plethora of physical evidence provided. Diuretics exacerbate the situation, working against your body’s desire to retain fluid to compensate.
- E – Classic Moro reflex, entirely expected and normal until it disappears around age 4 months
- E – I’m going to point out that a normal healthy kid with no cardiac history or symptoms and no family history of sudden cardiac death for a pre-sports physical is probably going to have a benign exam no matter what you think you hear.
- E – Pill-rolling resting tremor of Parkinson’s disease secondary to loss of dopamine neurons in the substantia nigra.
Requests for further clarifications etc can be made in the comments below. Your best bet for score correlations is probably here.
You may also enjoy some other entries in the USMLE Step 1 series:
— How to approach the USMLE Step 1
— How to approach NBME/USMLE questions
— How I read NBME/USMLE Questions
— Free USMLE Step 1 Questions
I don’t understand the gene rearrangement question. Could you provide a better explanation for that question? Also what would be a good score on this test if you’re aiming for 240+
The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation.
No one knows. I posted a score correlation link at the bottom of the page that you can check out which has estimates from both 2016 and 2017. Based on last year’s set, you’d be hoping for low 80s+
I think you copy pasta’d the explanation for the aspirin overdose from previous years. Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation.
I definitely did paste this from 2016, but the question is unchanged. The correct answer choice is B regardless. Note that whether metabolic acidosis combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows.
In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable.
How long till the respiratory alkalosis turns into a metabolic/mixed picture? Thank you for all the explanations!
12 hours is a good number to memorize but it can definitely happen much earlier.
From what I know the metabolic acidosis only present 12h post indigestion, while she is 3h only. what so you think?
It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). This question has been discussed in the comments of this post and the prior sets (2016 and 2014 I think). Regardless, the other answer choices cannot be correct.
But it was only 3 hours in this question and the answer was metabolic acidosis.
Again, it can happen significantly earlier. It usually happens by 12 hours.
Also, as a test taking point, time course aside, B had to be the answer. There was no choice for pure respiratory alkalosis. That is likely because if that choice had been available, the correct answer would be debatable.
Thank you so much for putting this together!
I think there is a mix-up with the sides for number 89. There is a problem with the right hypoglossal (tongue deviates right) and left lower and upper extremities.
The answer you have matches up correctly.
Thanks for the catch, it’s fixed now. That’s because this was a repeat question from 2016 including the same beginning and the same photo, but they adjusted a couple of things and flipped the side of the deficits, which I hadn’t noticed when I pasted in the old explanation. (They almost never adjust a repeat, oops!)
Question 89 – your explanation still stands but the sides are reversed. The question states left hemiparesis and right-sided tongue deviation which would mean a right-sided lesion (answer C)
Whoops, guess I didn’t refresh in forever and missed Michael’s comment. Thanks for your help!
Thanks to both of you. Fixed that–it’s a repeat question, but I didn’t notice they made the narrative a bit longer and flipped the sides from last year.
I just wanted to say thank you for all that you do. I found your website while studying for Step 1 and I read through all the question explanations/test taking strategies. Just got my score back and I’m happy with it, so I thought I would extend my gratitude, as your website helped a lot in my studying and that not too many people are willing to give out good information for free.
Ps – love the yearly reading lists and am excited to read your book
Thanks for the kind words. Speaking of good information for free, keep an eye on the site for the next couple weeks.
Thank you so much for your help during my STEP prep!
Found your site late in my prep but I’m definitely going to spread the word to others about this fantastic resource! Thanks Dr. Ben!
Hi Ben, thank you for this wonderful resource. I had a quick question on number 74, why can’t we assume that the patient with an elevated direct bilirubin does not have some sort of obstruction where the alkaline phosphatase would be elevated (or even dubin johnson syndrome)? I didn’t think of Gilbert disease despite the intermittent course because I tend to look at direct and total bilirubin levels first to see if the direct bilirubin is elevated which in this case was elevated.
Few things. History always comes first.
She also has even more indirect bili than direct. There’s also no other indication of obstruction clinically (such as pruritis), and you can’t infer an elevated lab value (alk phos) and rely on that in order to have everything come together. They have to give it to you.
Thank you so much, that helped tremendously!
Thank you so much for your consistent help! I am a new subscriber to your blog.
I’m taking my STEP1 in a few days. Wish me luck… this Free120 had some wishywashy questions imo.
I saw this question on Gilbert’s and also put down inc ALP. I noticed the relapsing-remitting history. However, my thoughts were that a direct bilirubinemia is a false finding in Gilberts (since it is due to lower UDP enzyme activity), and would more likely indicate obstruction. As you said, you would consciously neglect this finding in favor for the history?
For these specific NBME style questions – you know, the wishy/washy ones- would you follow the principle of “History first”??
Plethora of evidence first. Here everything points in one direction except one small detail. If you were to make a list of pro/cons for each diagnosis using history, physical and objective data (labs, imaging, etc), the scales usually tip firmly in one direction.
Came here to ask the exact question, glad you beat me to it!
Also came here to ask this exact same question, I guess I’m a little late to the party?
For question 115, would decreased cardiac output not also increase the blood pressure due to sympathetic activation of the baroreceptor reflex?
I think you’re ignoring a directly correct answer, increased PVR literally equals increased BP, and are instead trying to postulate an indirectly plausible answer.
Decreased CO, as you just implied, means less blood pumping into the aorta and less blood pounding and stretching the arteries and thus decreased BP. Note, your original logic would appy to stroke volume just as easily. Yes, a sympathetic response could then occur as a response to mitigate this, such as in shock or heart failure, but it would misleading to suggest that decreased CO causes hypertension.
Thank you so much Dr. Ben you have no idea how much I enjoy your straight-to-the-point, no BS style of writing. It’s hard to find as many clear educators as you nowadays. I would rate your level of teaching skill in the same league as Dr. Sattar. Cheers sir. You’ve got yourself a lifelong follower. Seriously, massive respect.
Q32 – platelet aggregation studies are normal- I thought they were abnormal in vWF disease. Can you or anyone please explain!
It depends on which kind of aggregation study and which type of VWD. This was discussed briefly on the 2016 discussion page.
Thanks Ben! Do you have explanations for step 3?
No sorry, I’ve never done any of the Step 3 sample question sets.
I eventually did.
Ben, are you planning to write explanations for step 3 or do you know if someone has done so? I figured out some diagnosis .. but confused about some other ones .. it would be great if you did an explanation for step 3 as well please.
I don’t think anyone else ever has. I’ve thought about it and I’d like to say I’ll start, but I don’t really have the bandwidth at this point, definitely not for the next month.
It’s alright. Take your time for step 3. As long as there is a good set of explanation.. it will be very helpful.
Hi Ben..thank you for your great work.
i was wondering where can i find the questions for the explanations you have provided ? is there a pdf version.i cant seem to find it anywhere.
Sure, there is a link to the PDF in the first sentence at the top of this page.
Thank you so much for putting this together. Can you please explain why B is incorrect for number 17?
Thank you so much!
B is the false positive rate, the number of people with a positive test but no disease.
Thank you so much for the prompt response!
hello again Ben and thank you for everything..is it possible to get uwsa offline? does anyone has a pdf version of it ?
I wouldn’t be surprised if someone out there does, but I wouldn’t know.
is there much difference in online and offline uworld ?
sorry for so many questions but new at usmle.
Any offline UW as far as I know would
be an illegal pirated copy. I have no idea how up to do date any particular available stolen version would be, but they defintiely won’t have any of the software features, test creation, question flagging, etc that are an important part of the product.
Can you walk me through 89 a little more for the other answer choices? I can’t seem to find a similar image online that describes exactly what those areas are covering. Thank you!
For an example, see Figure 6 from here. A and D, for example, would reflect lesions that cause what is called lateral medullary syndrome (Wallenberg syndrome)
Thank you. Would E then be the inferior vestibular nucleus based on that linked image? Also, is hypoglossal involved in the stem because of damage to the nerve fibers themselves rather than the nucleus?
I think the level in that example is a bit off from ours in the question. I assume they’re showing E as the hypoglossal nucleus (see this other illustration/article). Yes, it’s the fibers. The nucleus is ventral (as demonstrated in the new link).
Hi Ben, thanks for all the great explanations. For question 93, should we just assume that a pelvic fracture implies a membranous urethral injury? I was between membranous and spongy and I ended up choosing spongy because of the perineal bruising and fact that the patient was riding a motorcycle (and therefore susceptible to straddle injury).
Yes. You should think of spongy as the penile urethra, hence the predisposition to catheter-related trauma.
Just wanted to say thank you for providing these explanations! They have been extremely helpful. I also greatly enjoyed your piece on test-taking nonchalance. It has become my go-to as I take my Step in a couple of days. I look forward to reading more of you work as I progress through medical school!
Thank you SO MUCH for these explanations! So helpful!
The answer for number 14 “D. Microscopic examination of the stool” is correct, but the explanation is not. Cutaneous larva migrans, aka “pruritic serpiginous rash” is due to either ancylostoma duodenale or necator americanus, which can be treated with Bendazoles or Pyrantel Pamoate. Eggs would be found in the stool.
Moreover, for Strongyloides, larvae would be found in stool, not eggs.
Jk, you did say larvae and not eggs in your original post. mb :) (but I believe it should be necator/ancylostoma)
P.S. Thanks so much for putting this together. You are AWESOME!!! :)
I could be wrong, of course, but I don’t think so. I believe this is larva currens in the setting of strongyloides infection. Strongyloides, unlike CLM, explains the diarrhea, weight loss, and not just the eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil) with perianal involvement being significantly less common. Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason. See this nice comparison page.
Thanks for clarifying, Ben. It is easy to be led astray by the mention of a serpiginous rash, as most of the clinically relevant info you mention above is not included some of the more popular Step1 review material. First Aid 2018 only mentions serpiginous rash for hook worms… Luckily the correct dx wasn’t needed to choose the correct answer.
I do think that the main thrust of the question is to know the general type of organism and the likely treatment more than the specifics.
Thanks for this page Ben!
For question 101 I understand the breast feeding time period coming in for the lactose breakdown to galactose and glucose, but why coulnd’t Von Gericke be a differential aka choice D? Also could you explain the sugar testing a bit and what those are key for? Would they not be used in glycogen storage diseases?
Glucose oxidase test in the urine checks for glucose (where there wasn’t any because the child cannot produce any from the lactose). The reducing substance test checks for other non-glucose sugars like galactose, lactose, or fructose. These are used in the neonatal screen but are not helpful for GSDs.
So, the child in this case has a feeding intolerance and cannot convert milk into its useful component sugars. In contrast, von Gierke disease results in hypoglycemia and subsequent lactic acidosis due to the body’s inability to properly convert glycogen back into glucose for gluconeogenesis during periods of fasting.
Thank you so much for this wonderful source of information and explanation regarding the free 120 this year (and all previous years for that matter). I am taking the exam in 2 days so time is of the essence and didnt want to dig around on forums for the explanations, so your website has helped TREMENDOUSLY! It has been an immense help to fully understand the reasoning for the correct answers particularly in those that I got wrong.
I noticed that your website has a wide variety of information regarding Step 2, so I already bookmarked your website and will be a regular!
Again, thanks for the information.
Question 43;thank u for this website
Dressler syndrome occurs 》6weeks post MI (not 2-3wks)
Welcome. That is, however, not true. Classically the majority of cases occur after 2-3 weeks, though in real life 1-6 weeks is a better range.
Bustard’s gave same picture of kid finger in NBME 5 and there it was mouth, foot, hand disease :D. Just like they want to punish people who are doing old nbme :D ( picture was exactly the same and only RNA viruses were in choice). In conclusion NEVER trust picture’s !!!
Hello ben thanks so much for explicatons but i need to know about sample test usmle 2018 score conversion. Please let me know
I don’t think there are any for 2018 yet. You can see 2016 and 2017 for comparison though here: https://www.benwhite.com/medicine/step-1-correlations/
Hey just a heads up Question 8 Block 2 has been updated. Not sure about it but i think the answer is Tularemia treated with Aminoglycosides. Thank you so much for these explanations they really really helped me out alot.
Isn’t this the plague?
Do you know the origen of parafollicular c cells of the thyroid? In first Aid 2018 page 595 say that is the neural crest but in Uworld question 771 at the end of the table of the explication say that is the endoderm please let me know what is the correct o the best answer. Thanks again.
Endoderm from the fourth pharyngeal pouch. Neuroectoderm was what people previously believed.
Thanks a lot. Ben can you tell me what is the best order to do the nbme and uw self assesment. Let me know please. I am interested to know your opinion. Thanks again.
I don’t think it really matters regardless, but I’m probably not the right person to ask since I haven’t done all the NBMEs and the couple I did were over 8 years ago.
Thanks for compiling such an informative website. I was hoping you might be able to offer some insight into the way that you did calculations for question 27 (thalassemia inheritance), as when I diagram it out in a Punnett square, I keep getting an answer other than 50% for the two gene deletion. Wondering if I am missing something!
Mom: a-/bb (stem tells you she only has one gene deletion, arbitrarily chose a one gene deletion on gene a, her genes are the first vertical column)
Dad: a-/b- (he has to be this based on their description of microcytic anemia and two gene trans deletion, arbitrarily had gene 2 be “b” for clarity in counting, his genes are the row across)
a/b -/b a/b -/b
a/b aabb a-/bb aa/bb a-/bb
-/b a-/bb –/bb a-/bb –/bb
a/- aa/b- a-/b- aa/b- a-/b-
-/- a-/b- –/b- a-/b- –/b-
Shoot my Punnett square got all smushed when it went through the posting process…The top row (mom’s possible allele combinations) should be shifted right such that the first value is aligned with the second column!
So to avoid weird formatting, let’s just use
Mom: BAD GOOD
Dad: BAD BAD
Possible combinations: BAD-BAD, GOOD-BAD, BAD-BAD, GOOD-BAD
Out of the four combos, two are two gene deletions.
That’s the right answer. But wouldn’t that be an oversimplification since there are two alpha genes with 2 alleles per gene?
How would you define the components of the serum sickness reaction in question 47? I thought since the female has bone marrow failure and is receiving antithymocyte globulin (idk why she would get this anyway), she has no functioning B-cells and therefore cannot develop a antibodies to foreign proteins. Wouldn’t she need functioning APCs, mature T cells, and mature B cells to generate a serum sickness reaction?
Antithymocyte globulin is sometimes used in bone marrow failure conditions like myelodysplastic syndromes and aplastic anemia. It can also be used to prevent a bone marrow transplant rejection. That’s beyond the scope of the test; the salient point of the question is that it’s from a rabbit.
Bone marrow “failure” doesn’t mean she has literally no immune syndrome. It means that the bone marrow isn’t able to produce enough for all of the body’s demands. There’s a spectrum of severity. Just like heart failure doesn’t mean your heart has stopped pumping entirely.
Hi Ben, Thanks for your amazing work here. super helpful and convenient!
I have a question about question 57 on CGD. why is the answer “intracellular bacteria” ? first neutrophils are phagocytes mostly kill bacteria that are extracellular and have only maybe a small part in extracellular pathogens, no? secondly all the catalse positive bacteria are not even facultivate intra-cellular… what’s your opinion on that?
Thanks again, Yoav.
They presumably mean ‘intracellular’ in the more mundane sense that once a neutrophil phagocytizes an organism it is by definition “inside” the cell. They probably could have said “ingested” to be clearer.
Thank you for such comprehensive explanations! For question 5, could you explain further why P-selectin is not a possible correct answer, for its roll in rolling during leukocyte extravasation?
Question asks what’s causing the “formation of this tissue.” Single best answer. Doesn’t meant the wrong choices are not involved or irrelevant.
P-selectin may be involved in platelet and white-cell recruitment but does not cause granulation tissue formation etc
Hey Dr. White,
I just want to say thank you for these resources. They are truly amazing. I had a quick question on #64. The answer is “thyrocervical trunk.” However, why wouldn’t a branch of the external carotid also be a valid answer? Does the superior thyroid not also give arterial supply to the parathyroid glands? It seems to me that it could be either of these.
Thanks in advance!
Superior thyroid provides mostly collateral support. The inferior thyroid is the primary supply and thus the “single best answer.” Remember, the other answers don’t have to be wrong to not be the best.
Thanks for the clarification!
I guess I am confused on #50. Wouldnt a P450 inducer like carbamazepine increase the activation of VItamin D since it “induces” the CYP450 system?
More complicated than that. The CYP450 system is indeed involved in Vitamin D bioactivation via 25- and 1α-hydroxylation, but it is involved in its catabolic breakdown into inactive metabolites. If you’re curious, see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3927478/
Thanks so much! that helped clarify my confusion.
Thank you very much!
First of all, I want to thank you for such and amazing and constant work through out the years, this has helped me a lot.
I just wanted to point out that on question 48 I believe that the question is referring to Y. Pestis. It’s kinda funny because it turns out that, indeed, both diseases are treated with Streptomycin.
And again thank you very much!
I agree, please see the 2019 explanations for more discussion. The similarity is not a coincidence. Both are caused by gram negative bacteria transmitted in similar ways and often causing a similar clinical picture. As a result, they are often discussed together. I think it’s perhaps no surprise that the question hinges on a shared treatment and not the diagnosis.
Oh, cool. I just read it. Yeah, you are right, it is no surprise. Also loved the couple of historical facts you thrown there. T
regarding hearts sounds question , i want to add that in pulmonic area there is an S3 and i was sure it was an S3 , i wasn’t sure how does is collerate with P.HTN thouhg but i picked it anyway which is wrong …
immediately there after i remembered , S3 heart sound is NORMAL finding in adolescent and pregnant patient ….nice question
Are you sure it’s not simple A2/P2 splitting–especially given that it increases with inspiration?
Thank you for this exceptional resource. Regarding the unstable angina/nitrate question, would you be able to further elaborate on why nitrates are the correct choice? The question states that the man has an S4 which can be seen in HCM, and nitrates are contraindicated in HCM in my understanding. Are they okay to use at least in the acute setting such as this but not long term?
Way overthinking it, I’d say. S4 is not even something to jump to HCM for in a random 50-year-old man who is presenting for the very first time with classic signs of coronary ischemia. S4 is often used a suggest acute ischemia or diastolic failure (of any kind, not just HCM) on questions. If a guy like that comes to ER, he’s gonna get at least MONA (I don’t care what his clinical heart exam looks like).
You took a giveaway easy question and tried to make it a trick question. As a general rule, don’t do that.
Main nitrate contraindications are erectile dysfunction meds, hypotension, large pericardial effucion, large RV infarct, or severe aortic stenosis.
Thanks SO much!
A few questions:
For #70 – doesn’t H. Pylori stimulate gastrin secretion as well, increasing acid and thus inducing ulcers? If so, can you explain why answer “B” is wrong?
For #48 – I was thrown off by the picture, which doesn’t show bite cells or Heinz bodies–it looks more like schistocytes or potentially sickle cells. I know the stem points to G6PD, but can you help me understand the picture?
#70 Hypergastrinemia, as a result of the antral mucosal damage, is thought by some to play a role in downstream duodenal ulcers. But the stomach ulcers are not a result of globally increased acid production, no.
#48 They’re just schistocytes. People with G6PD get hemolysis when acutely triggered, as the patient in the vignette was by Bactrim.
Hey Ben, thanks so much for putting all this together. I had a question about 95. the kid with herpes (oral vesicle and hand lesion). I was thinking it was Coxsackie virus since lesions were present on the hand and mouth (not foot though) and primary HSV-1 lesions tend to be more severe (herpetic gingivostomatitis, a la UWorld). So I was stuck between choosing hand foot mouth disease with no foot or uncharacteristically mild primary HSV-1 infection that affected both the hands and the mouth, not just one. I ultimately thought coxsackie fit the picture better. Do you have any insight on how I could have picked herpes instead?
While HSV1 can certainly be devastating in the form of herpes encephalitis, most cases are mild. Keep in mind most people are asymptomatically infected as children and don’t even know it. Children can sometimes autoinfect their fingers from their own oral lesions (aka thumb-sucking), as in this case.
HFMD is a common childhood illness where the kids display fever, prodromic symptoms, often poor appetite, blah blah blah. Isolated rash in exactly two spots without anything else would be unusual.
For question 113, how is the correct answer “lifelong persistent infection” correct when we have treatment for Hep C? Does hep C not come and go (answer B “latent infection with intermittent viremia”).
Just because there is a treatment or potential cure for a disease doesn’t change its natural history. Hep C is never a latent infection with intermittent viremia. It’s not a virus like Herpes or Varicella that infects a host and then lies dormant until episodic reactivation.
First of all. This explanation is legendary. You’ve saved me so much time in the few days leading up to my step exam. Question on #69 though. Every source I look at says that (E) Vancomycin the the appropriate treatment for MRSA, yet you list (D) Rifampin. Is there something that i’m missing here? Thanks in advance.
That was one of two new questions changed in the 2019 set, see the explanation updates here: https://www.benwhite.com/medicine/explanations-for-the-2019-official-step-1-practice-questions/ (the other one was changed on this set mid-year and is reflected above)
But yes, the answer on the 2019 set’s question 69 is definitely E (vancomycin). This page is technically for the almost identical 2018 set.
Can’t thank you enough for making this. Incredibly helpful.
First I want to say thank you so much for taking the time to do this!! But I was wondering, some of the answers have a * symbol at the end- does that mean anything specific?
The asterisk means that the question was new since the prior year.
Awesome Dr. White! Thanks a bunch. Got the test in 2 days. You’ve been a huge help.
For question 94, how do you tell apart HSV vs. Hand foot and mouth? Dont they both have lesions in the mouth and hand/fingers?
It’s actually not necessary to have to have HSV simultaneously on the hands and mouth. It would be very uncommon to get it on your feet.
For Question 108. Aren’t nitrates contraindicated in patients with HCM?
See comment above. Overreach to assume HCM in this context.
Your attitude and answer explanation were a joy to read and go through! Boy the whole time i was solving UW and NBMEs i said these things to myself and now i’m glad that i’m not the only one who thinks like this to narrow down and pick right answer choices!
Haha.. loved the experience. Will definitely recommend this blog post to more people. :)
Hi. Thank you for the post!
Why would Block 1 Question 32 be von willebrand disease when platlet aggregation studies are said to be normal in the labs?
Depends on the kind of aggregation studies (and the kind of VWD). See discussion in comments at https://www.benwhite.com/medicine/explanations-for-the-2016-official-step-1-practice-questions – USMLE historically loves bleeding time for VWD.
I missed this question because PTT was normal. Pathoma says vWF stabilizes FVIII so VWD causes an increased PTT. Is that not true? or something that can happen, but doesn’t have to?
The latter (can happen but not something to be relied on). There is more than a single monolithic VWD, and so while platelet aggregation time (or on tests the somewhat unreliable low-tech “bleeding time”) is the best test, in reality, the idea is that you don’t need a diagnostic lab abnormality to have the disease.
thank you so much for your job!
9 – why not A?
71 – why could it also not be C?
75 – wouldn’t you expect annular pancreas to be in a newborn? Anything else that clues us into this NOT being SMA syndrome? I feel like in both there would be weight loss, vomiting, dilated stomach/duodenum.
107 – why not A? – seems like this is also describes the “double hit” hypothesis?
9. Affinity maturation is the process by which T cells produce more efficient antibodies, which typically happens with either somatic hypermutation and clonal selection; this is not the gene rearrangement. The tag here is for an antibody constant region. As Mayo says, “As B-cells develop, the segments are rearranged such that each mature B-cell and plasma cell has a unique rearrangement profile. Other cell types usually retain the nonrearranged gene structures.”
71. Because B is true by definition and is, therefore, the best answer. Also, the evidence suggests that it has no significance.
75. No, it’s commonly seen in adults and can even be totally asymptomatic. The CT image shows a completely normal interval between the aorta and SMA without compression.
107. It’s not just the pancreas involved, this is a germline mutation process.