The NBME has released the new 2016 “USMLE Step 1 Sample Test Questions,” which reflect a sizable decrease in the number of questions from 308 down to 280 and now 40 questions per block after May 9th, 2016. Exam duration is unchanged, so this should help those who have difficulty with time management/finishing sections on time.
Additionally, on the software package, you can now invert the colors for white text on a black background. If that’s your thing.
You’ll remember from last year that there weren’t any new questions. This year there are 49 new ones (marked with asterisks).
The questions and explanations for last year (2014/2015) can still be found here.
- D – ITP causes immune-mediated consumption of platelets, hence the low platelet count and petechiae. The bone marrow biopsy results demonstrate that the body has appropriately increased platelet production, meaning that this is not a platelet production issue. While TTP has a similar acronym, it’s an entirely different disease with a classic pentad: thrombocytopenia (low platelet count), microangiopathic hemolytic anemia, altered mental status, renal failure, and fever.
- A – Crystal disease of the knee is mostly commonly pseudogout (aka calcium pyrophosphate deposition disease / CPPD). Contrast with gout which most commonly first affects the great toe MTP. These crystals would be positively birefringent (not mentioned). The radiographic features are microdetails that are unlikely to make or break the diagnosis on your test.*
- 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.
- D – Of the choices, only Shigella is a common US pathogen causing dysentery (bloody diarrhea). Shigella is extremely virulent, and a handful of organisms is enough to cause infection, with the misery-inducing Shiga toxin being similar to the toxin produced by enterohemorrhagic E coli’s O157:H7 strain that can result in hemolytic uremic syndrome.*
- B – Alcoholics (and any person with an altered level of consciousness) are a set-up for aspiration pneumonia: classically RLL, classically foul-smelling. The organism on tests will be Klebsiella.
- 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.
- 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.*
- B – This patient has cystic fibrosis. The combination of respiratory and GI issues is classic and caused by ineffective chloride transport and consequently thick exocrine secretions, which clog up the airways and the pancreatic ducts.
- G – Great example of a long-winded set up for a heart attack followed by the giveaway diagnosis of heart attack (*cue moan for wasted time*). Beta blockers are given to reduce myocardial oxygen demand and thus reduce ischemia by slowing the heart rate and reducing contractility.*
- 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 – 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.
- 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.
- 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 know to get the question correct).
- D – If the patient was positive for HIV, then the wife must be informed. In the absence of the disease-related exposure, this is none of your business. Private health information is private.*
- 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.
- B – Isoniazid is hepatotoxic and can cause serious liver damage. Highly testable. It can also cause drug-induced lupus (which is probably even more testable).*
- B – Albuterol (inhaled short-acting beta2-agonist) is the treatment of choice for wheezing/reactive airways/bronchospasm/asthma. Note that timolol is a beta-blocker and beta-blockers can cause bronchospasm/exacerbate asthma. Even eye drops.*
- 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.
- C – If you don’t eat enough calories to run your metabolism, your body will mobilize its stores. We “burn” fat through fatty acid oxidation.
- 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).*
- 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.
- E – The whole afferent/efferent thing is worth knowing. When the efferent arteriole is independently constricted, the blood can get into the glomerulus but has difficulty getting out. So more blood spends a greater amount of time in the glomerulus being filtered: GFR up, filtration fraction up, but overall blood flow is decreased due to the increased resistance of the system as a whole.
- 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.*
- A – The infraspinatus and teres minor are responsible for external rotation. Both the infraspinatus and supraspinatus muscles are innervated by a suprascapular nerve.
- B – Type I hypersensitivities aka “allergies” (as seen in snot, hives, and eyes) are mediated by IgE (mast cells, basophils).*
- 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).
- A – GBS comes from a mother’s colonized vagina and is the most common cause of neonatal sepsis. Women who are GBS+ should receive PCN prophylaxis prior to vaginal delivery to prevent exposure to the fetus on the way out.
- 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.*
- B – You want this to be a CYP450 question but it’s not. Some drugs require an acidic environment to be satisfactorily broken down or dissolved for GI absorption. Omeprazole raises gastric pH and reduces GI absorption.*
- A – All the vesicles contain the same viral infection, so all should have the same appearance on gel. Choice D is what a gel looks like without using a restriction enzyme digest (no discrete bands of specific weights).
- C – Effects of PTH – Raise calcium and vitamin with an overall decrease in phosphorous (due to decreased urinary resorption).*
- B – Juxtaglumerular cells secrete renin when their beta-1 receptors are stimulated. Blocking the JGA reduces everything in the cascade, including renin. Blocking anything later in the RAAS pathway would cause an elevation in renin as an attempted compensation.*
- D – Knowledge of the normal cavernous sinus contents and all of the cranial nerves and their functions is low-hanging fruit. Ocular ABduction is mediated by the ABducens nerve, CN VI.
- D – Losartan is an angiotensin II receptor antagonist used to treat hypertension by blocking the effects of angiotensin II and reducing aldosterone production. Vessels relax, sodium is less held onto, which results in decreased blood pressure via the decrease in the peripheral resistance and preload.*
- 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 – 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).
- 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.*
- B – Memorize aspirin’s acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.
- C – Most “biologics” are monoclonal antibodies. Infliximab (remicade) and adalimumab (humira) for example both block TNF-alpha and are both antibodies (end in “mab” for monoclonal antibody). As such, the body can eventually form an immune response to the foreign protein.*
- 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.
- 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.
- D – Those are varicose veins, and they’ve described symptomatic varicosities. Incompetent valves allow reflux of blood into the dependent feet and legs. The pooling blood increases hydrostatic pressure, causing edema.
- F – This question is so easy it almost defies logic. Treatment of choice is pyrimethamine+sulfadiazine (and folate). Unlikely to be tested, but the differential for a ring-enhancing lesion in an AIDS patient is CNS lymphoma (which is more likely to be solitary). In real life, one can do a thallium or PET scan to distinguish the two (lymphoma, being cancer, is metabolically active; the toxoplasma abscess is not).*
- E – Kidneys hold onto salt and fluid in the event of volume loss.* Vasoconstriction certainly occurs to maintain blood pressure, and while this is related to RAAS, this is not the “best” answer, because the kidneys aren’t doing the constricting; the vasculature is.*
- 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.*
- 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).*
- 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 – The vast majority of pancreatic cancers arise from the ductal epithelium (>80%), possibly due to long-term exposure to lots of potent secretions. Acinar epithelium is responsible making exocrine secretions. Islet cells can form neuroendocrine tumors (insulinomas).*
- A – Turner syndrome (you may remember lymphedema of the neck by another name: cystic hygroma). The 45,X gives it away though anyway. Mosaic Turner’s syndrome and the mosaic trisomies result from nondisjunction during mitosis. In total monosomy/trisomies, the cause is nondisjunction during meiosis. Uniparental disomy is essentially only tested via the Prader-Willi and Angelman syndromes (chromosome 15).
- 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.*
- C – Lymphatic spread of disease moves through lymphatic channels from distal to proximal. The medial side drains to the superficial inguinal nodes. Much of the lateral side will stop at the popliteal nodes prior to ascending the thigh.
- 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.
- F – The statin is saving 10 people per 1000. Good numbers for easy math. So we need to treat 100 people to save 1, at a cost of $1000 x 5 years per patient. 100 x $5000 = $500,000 (F).*
- B – Crossed findings means a brainstem lesion. Left (ipsilateral) tongue, right-sided (contralateral) weakness means the exiting left hypoglossal nerve has been affected (within the left medulla). B 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.
- 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).
- D – Adult polycystic kidney disease (APKD) is autosomal dominant. Thus 50% of their kids will get it.*
- A – The closer R is to 1, the more closely the data points should fit to a line. I think the NBME is trying to imply that I will have poorly controlled diabetes in the future.
- A – Pyknosis and nuclear fragmentation are part of the process of apoptosis.
- A – An annular pancreas occurs when the pancreas is wrapped around the second (descending) portion of the duodenum. When symptomatic (in adults, typically when there is superimposed pancreatitis), it can block the flow of GI contents through the intestines.
- D – Recurrent respiratory infections could be a lot of things. But then they mention the dextrocardia. Kartagener syndrome is the combination of situs inversus and defective cilia (due to a mutation in dynein), where the inability to effectively clear secretions results in recurrent sinusitis and bronchiectasis.
- 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 development 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.
- 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.*
- C – Serum sickness! A type III (immune complex) hypersensitivity.*
- 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.
- 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.
- D – No B cells and their antibodies. No CD4 or CD8 T cells. So both limbs are out: SCID. DiGeorge syndrome also has missing T cells and no thymus, but B cells are present (though less effective without helper T cells).*
- 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.
- D – The suprachiasmatic nucleus of the hypothalamus controls circadian rhythms. A few more key thalamic nuclei are worth knowing: Supraoptic releases vasopressin (ADH). The lateral nucleus controls thirst and hunger. The ventromedial controls satiety. Anterior controls temperature. The paraventricular nucleus releases CRH, TRH, and oxytocin.
- 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.
- A – Narcotic use for acutely painful conditions is both reasonable and important. Short-term use (immediately post-surgical) does not lead to long-term dependence. And yes, drugs addicts should also receive narcotics to control pain.
- C – Logic would dictate that a fracture of the inferior orbital wall through the infraorbital foramen might affect the infraorbital artery, and logic would be right.
- 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 – The Pouch of Douglas is the space between the uterus and the rectum (i.e. the place where pelvic free fluid goes).*
- B – Crohn’s: skip lesions, fistulae, strictures (and the unnecessary transmural involvement on histology).*
- 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 – Antibiotic-associated diarrhea caused by clostridium difficile can be tenacious, difficult to treat, and even fatal. Alcohol-based rubs are not sufficient to kill the spores. Handwashing with soap is necessary, and equipment should be autoclaved to clean it.
- 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. Austism-like behaviors and relatively large head are common; large testicles only appear after puberty.*
- 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 – He’s clearly in heart failure, so one wants to know his EF to determine between systolic versus diastolic and establish pretreatment baseline.*
- D – Diffuse low-level ST elevation means pericarditis. These patients often complain of pleuritic chest pain, which 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).
- 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.*
- C – Leydig cells make testosterone. Leydig cell tumors aren’t always physiological 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.
- B – Annular lesions with central clearing is a good appearance for Tinea corporis. Superficial fungal infections induce a T-helper response that results in class switching to IgE-producing B cells (mediated by IL-4), which can exacerbate atopic conditions.*
- 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.*
- A – Acetaminophen (Tylenol) can cause fulminant hepatic failure in overdose. This will probably be on your test.
- 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).
- B – This is a (prospective) case series. There is no control group (and certainly no blinding).
- C – If an adult is taking on behaviors common to children, it’s called regression (don’t feel bad if it’s something you might do yourself).
- 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.
- 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 – 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).
- A – Beta2-agonists like albuterol are the treatment of choice for acute asthma symptoms/exacerbations. This question is stupid.*
- 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.
- 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 lifecycles are gross.*
- E – Subacute combined degeneration (progressive peripheral sensory and motor loss) is a late sign of B12 deficiency, which is common in old people. On board 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 – Neutropenia most commonly predisposes to overwhelming bacterial infection. It may also be worth noting that patients with neutropenic fever must be covered with an antibiotic that covers for pseudomonas (e.g. pip-tazo, ceftazadime, or cefepime).*
- 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.*
- 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.*
- 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). *
- D – Schistosomiasis is a parasitic worm particularly endemic in Africa (Egypt in particular comes up a lot 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).
- C – Run of the mill neonatal jaundice is due to a build-up of indirect/unconjugated bilirubin and is essentially a physiologic finding in newborns due to the combination of fetal erythrocyte breakdown and transiently low hepatic excretory capacity. Particularly high or rapidly uptrending levels are treated with phototherapy due to the risk of kernicterus. Breastfeeding jaundice and breast milk jaundice are two additional etiologies of neonatal jaundice, both of which also result in indirect hyperbilirubinemia.*
- A – Foot drop after compression in the lower leg = common fibular/peroneal nerve. Nerve compression syndrome = one reason why it’s important that casts not be too tight.
- 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 – 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.
- 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).
- G – Sulfonylurea medications (glipizide, glyburide) stimulate the pancreas to secrete more insulin. For this reason, they are most efficacious early in the disease process when pancreas still has remaining functional reserve.
- E – Those are sickle cells on the smear. LUQ pain on test questions almost always means splenic pathology. All sickle cell kids will eventually infarct their spleen.
- E – Functional parathyroid adenomas can cause elevated parathyroid hormone (PTH), which results in hypercalcemia and hypophosphatemia. Hypercalcemia is characterized by the rhyming symptoms of: 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).
- 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.
- 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 artery pressure is significantly elevated.
- C – Blood flow also increases during exercise. The more anaerobic metabolism you use and lactate build-up you have, the more hyperemia you need to clear out the waste products.
- E – Ventricular fibrillation is the most common cause of sudden cardiac death immediately after myocardial infarction. This is why we have AEDs all over the place now. Papillary muscle rupture classically occurs 2-7 days after an MI and results in massive life-threatening mitral regurgitation. Free ventricular wall rupture after an MI can result in cardiac tamponade.
- C – RSV, like all respiratory viruses, spreads via respiratory droplet. Babies are too young to wheeze because of asthma; they wheeze because of RSV.
- B – Head injury follow by the copious dilute urine means central diabetes insipidus. No ADH (made in the supraoptic nucleus of the hypothalamus, secreted from the posterior pituitary) means no aquaporin channels in the collecting ducts to resorb water.*
- C – GVHD sucks. Skin and GI lesions are especially common sites (mucosal tissues are rapidly dividing and thus prone to attack).
- A – p53 is the quintessential tumor suppressor (it activate apoptosis). Carcinogenesis of HPV is caused by insertion of the virus into the host DNA and producing a protein which binds to an essential p53 substrate, functionally inactivating the p53 and its apoptotic cascade. C (transactivation/TAX) is how HIV and HTLV cause cancer. E (cmyc translocation) causes Burkitt lymphoma.
- F – The flexor surface rash is eczema. Pimecrolimus (like tacrolimus) is an immune-modulating drug that suppresses T-cell cytokine production.
Requests for further clarifications etc can be made in the comments below.
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
Thanks so much!
I think question 62 is a case of accessory nipples & not pubertal gynecomastia. Doesnt matter anyway. Thanks
Nah, I very much doubt it. “Beneath” in this context means “deep to” not “below” (as you would expect to describe a location on the nipple line). The question even asks for the explanation of bilateral breast enlargement. Accessory nipples, even if they have associated glandular tissue, would rarely be mistaken for normally located bilateral breasts.
Thank you very much these are incredibly helpful!
Do you think the new changes to the USMLE will make it harder or shift grades down? If a student is hitting his/her target NBME just before the change any reason to wait for the new version or better to stick with the old?
No, I think things will be essentially unchanged. The fewer questions should make the test a bit shorter and possibly easier (at least for those struggling with time management), but I imagine the change is really designed to account for some of the lengthier question formats that take more time. Any impact this has should be normalized away, so unless test fatigue etc are a big problem, I would just take it whenever convenient.
is it possible to get a 3 digit correlation approximation from the percent that was correct here
I don’t think so at this point. People had tried this many years ago, but the questions have changed and I don’t think it’d be helpful to use their results. If people share their scores before and after, that might help, but only if the data comes from people who use the questions in close proximity to their exam date.
Thank you so much for explaining all of these answers. How representative are these questions compared to the actual step 1? (easier/harder/about same). It seems biochem, micro, and repro are my weakest subjects. Other than reviewing these modules, what else can I do within 1 week prior to the exam for most efficient time usage?
Thanks again for prompt response and everything you do on the blog.
I think they correlate about the same overall. A lot of easy ones, some hard ones, a few crazies. Within a week, I’d make sure I had mastered my mistakes on UW. If you feel you have exhausted the qbank of its mysteries, you could do a few NBMEs to simulate the real deal early on. I’d try to take it easy the day or so before and memorize random facts (cytokines, enzymes, etc) and conserve your strength.
39 – is Etanercept another TNFa inhibitor that meets this description, or are there distinctions between it and adalimumab and infliximab?
Yes, Etanercept is not an antibody (the immune response to a foreign-derived antibody is the crux of the question). You can always tell one by the name (-“ab”), as described above.
Thank you so much! I have to say, your explanations are perfect. Wish the qbanks would explain it this discreetly without giving me a whole textbook description sometimes. Not to mention the humor you added to the explanations.
Thanks, glad they’re helpful!
I couldn’t agree more. Ever thought about creating your own question (and perfect answer) bank?
Intermittently (and mostly briefly) considered the idea of both a book and a question bank. But the practical matter is that doing either one right would be a massive undertaking. There’s a reason most of the books you see are usually written by committee (even if only one author is on the front). If I had been more industrious I could probably have done one while going through school, but sadly my intrinsic nature of multilayered procrastination prevented that when the time was available.
For Question 20: if displacement was an option- do you think this scenario would be an example of displacement?
Thanks so much for posting these! Very helpful!
Not the best example, no. Displacement is classically described when a person diverts (“displaces”) an unacceptable negative emotion/action from the true recipient to another in order avoid anxiety/negative consequences. My favorite illustration: an attending yells at a resident. The resident, unable to yell at this boss, yells at the medical student (a much safer victim). In this case, if anything, yelling at your children (who are contractually obligated to love you) would be less problematic than yelling at a patient.
And then who do the children yell at?
Ah, they act out in restaurants and on airplanes.
For question number 9, I was wondering if no change in heart rate with decreased contractility and O2 utilization would also be an acceptable answer. Just trying to reason out why one would choose one over the other. The stem mentions that the patient was also given nitroglycerin which would cause tachycardia. Giving a beta blocker would eliminate the reflex tachy, but would it cause a decrease in the heart rate?
In real life, there are always a lot of factors at play, including how much of each drug a patient is getting. That’s beside the point: the question is specifically asking what are the likely effects of an intravenous dose, which means they are specifically asking you what metoprolol does. So I would say the answer to your question is no.
To answer your second question, metoprolol definitely decreases HR in the setting of nitro use. For coronary CTA, for example, we actually give nitro to dilate the coronary arteries and metoprolol to reduce HR and it works like a charm.
Thanks for your explanations. They truly helped me a lot. Concerning the nitro and b blocker combination I had the same question since first aid (2017 edition, pg. 305) mentions that b blockers and nitrates combined have NO EFFECT or decrease in heart rate…
I have to imagine they meant there is no synergistic effect. The idea that the two perfectly cancel out in combination in all situations would be sort of ludicrous?
Thanks so much… i got 27 wrong out of 117 which would be around 77%. I’m an italian doctor hoping to go to the states….
Is the result any good for someone who wishes to take the exam pretty soon? I’m praying for > 230
No one knows the correlation, but if I had to guess I’d put that in the 210-220s range. The NBME exams you can buy/download have better score predictions.
For block 1, question 38: how do you determine that the pH decreases? I thought that respiratory alkalosis was usually an early response, followed by metabolic acidosis.
Thanks for your help!
For one, I’ve never seen an ASA question that didn’t test the classic combination. But more importantly, the case here is that pure respiratory alkalosis isn’t an option. If you want pH to go up and pC02 to go down early in the time course, that’s fine. But the choice for that here also has bicarb going up, and you don’t have a superimposed metabolic alkalosis with ASA toxicity. If the time course they provide in the question doesn’t help, the answer choice options absolutely will.
Sounds good. Thanks!
C – Effects of PTH – Raise calcium and vitamin with an overall decrease in phosphorous (due to decreased urinary resorption).*
Patient had chronic kidney disease aka secondary hyperparathyroidism, which means kidney is unable to excrete phosphate AND unable to make activated Vit D. The answer is increased PTH, decreased calcium, decreased phosphate, and decreased Vit D.
Oops disregard…this wasn’t even a CKD question. I was going off a group compiled list (no 2016 NBME practice simulation for MAC users yet). My bad!
No worries. I have a Mac too, which is unsupported. I just use the PDF, which has everything but a few interactive questions.
are these xplanations of nbme 18?
No, these are for the free USMLE practice materials, which are updated annually. The NBMEs are tests that you buy individually, of which several are for sale at a time.
Just took step 1 and I can’t thank you enough for these explanations! Only wish I would’ve found your site earlier on in my studying. Keep up the great work, sir!
For q 56, How do you assume that the man is heterozygous? not homozygous?
Because they dont actually give any info on the parents of the man?
For autosomal dominant diseases, any parent with the trait will express the disease. For the patient to be double dominant, that would require both parents to have adpkd, something that you would never assume without being explicitly told. Additionally, homozygous adpkd typically has a more severe course and earlier presentation.
Lastly, as a default, consider all cases of AR diseases on tests to be from two asymptomatic carriers and all AD cases to be heterozygous. The classic exception/test question concerns double dominance achondroplasia, where homozygosity (resulting from the union of two healthy achondroplasts) is uniformly fatal.
Would you clarify please #23?
Even if 1 X-chromosome is inactivated, wouldn’t both X chromosomes be involved in oogenesis? Don’t they have to be involved in order to have 4N to start off with?
You are correct that x-inactivation doesn’t play a role in gametogenesis (in women).
The point of the question is that we don’t know based on the clinical history provided whether or not the patient is a carrier or not. Her mom is, but she may or may not be. Her normal CK doesn’t exclude a carrier state; the degree of disease for X-linked carriers depends on X-inactivation (which is usually 50/50, often resulting in an asymptomatic state, but can also be skewed, sometimes resulting in better or worse phenotypes).
You are the best,Ben! Thank you so much
Hi, I’m glad I ran into this as I just did these questions. Are those questions representative of the actual USMLE? It’s that I’m a little confused as I did an NBME and didn’t do all that great but in these questions I actually did good, So now I’m not sure what to think. Thanks!
I think they do probably both correlate well. The real thing is a mix of easy, medium, hard, and absurd questions. I think this has fewer of that last category, but regardless all of these exams are standardized, so the grading takes into account if the series is on the easier or harder side of the USMLE spectrum.
Thank you so much for taking the time to explain each question! Glad I stumbled across this site.
I have a question for number 53 though. It says ” The statin is saving 10 people per 1000″. Is this by any chance just a typographical error (10 instead of 100)? :)
I don’t think so, how does this sound? There are ten fewer fatal MI in the treatment arm versus be placebo arm (which each have 1000 subjects). So it’s saving 10 people out of the 1000 treated by the statin, meaning we need to treat 100 people to save one.
Oh I’m so sorry! You’re right. I made a mistake by calculating ARR (c/c+d)-(a/a+b), which ultimately gave me 100 too. But your explanation is much more simple. Thanks so much!
I just don’t see it! Please help!
Yay!! I see it!! So simple!!
hi, could you pls explain question 81……… why the platelet aggregation test is normal in VWD? my problem is that Gp1b and VWfactor have to interact to induce a confirmational change in platelets to release ADP –> ADP binds to adp receptor and induces Gp2b/3a which enables aggregation via fibrinogen. which would lead to abnormal aggregation?
and is the ristocetin assay not a platelet aggregation test ?
or can it sometimes be normal and sometimes not?
It can be abnormal as well, depends on the subtype and severity (the wikipedia page does a decent job explaining). The most common subtype of VWD is a quantitative defect, which is often mild/nearly clinically occult and can have essentially normal laboratory testing. This is one of those questions where the labs are really there to exclude the other choices.
thank you so much :) yes I saw the wiki page…..I had only heard of platelet aggregation test being abnormal before taking the online evaluation and that’s why I excluded the option. now I know all the subtypes :) thx again
Thank you so much for sharing these explanations and additional tips! They are incredibly helpful!
For Block 1 Q35 about Hep C, choice C (lifelong persistent infection) makes sense as the answer, but why is choice B (latent infection with intermittent viremia) wrong?
Latent infection with intermittent viremia is more analogous to some cases of HIV, CMV reactivation, etc. Latent infection is like when chickenpox hangs out in the dorsal root ganglion before reactivating and causing shingles. Hep C is always active; it just doesn’t always cause enough damage to lead to cirrhosis.
Thanks a bunch!You just saved me so much time and the humor in the explanations helped soothe my nerves a bit :) A week to go and a bit panicky! Any advice for a last run through FA ?
If this late in the game it feels like you’ll just never remember something no matter how hard you try, then don’t learn it. A random biochem fact that you can’t pin down isn’t going to cost you more than a question or two tops (and probably won’t be on the exam anyway). Call it a loss with a smile. A positive attitude is paramount at this point in all your test-related endeavors—this is the end!
hey thank you very much for the effort..
regarding q-38. after aspirin overdose- isnt it respiratory alkalosis at an early stage and metabolic acidosis in a late stage?
(in the question it was 3 hr- early stage ) can you explain why isnt the answer C? which says pH increases, Pco2 decrease and bicarbonate remains same or a bit elevated – which matches respiratory alkalosis?
you wrote that the answer is B which has low pH.
Someone asked a similar question last year (it’s a repeat) as to why if it’s early it’s not just respiratory alkalosis as opposed to the classic mixed respiratory alkalosis/metabolic acidosis. Here was what I told them:
I’ve read 3 hours in the past as the cutoff for mixed, but more importantly, I think you’re overthinking it. I doubt you’re ever going to see a question in real life that hinges on that; ASA toxicity questions are most likely to test if you know the classic mixed metabolic acidosis/respiratory alkalosis. Bicarb down, pc02 down, and pH down (though mixed, the metabolic acidosis tends to dominate).
Note that C is wrong no matter what. Bicarb going up would be metabolic alkalosis, which you would see neither in ASA overdose nor as compensation for respiratory alkalosis. In this case, you’re chasing the pH because you want the patient to be alkalotic, but the answer choice is internally inconsistent.
ok then, thanks!!
Hey Ben, I could be misunderstanding this concept, but couldnt it be that the HCO3 is up because the kidneys havent started compensating yet? Thus the HCO3 is still high? And pH is high since it is a respiratory alkalosis at first? I thought 12 hours was the cutoff
The metabolic acidosis is not a correction to the respiratory alkalosis. Furthermore, if the kidneys haven’t started compensating, following that logic, then the arrow would be neither up nor down. It should be normal.
pH is down (not high) in the correct answer choice according to the question.
Ok, thank you for your response
One more question for you: looking back at a U world question, the explanation states that the metabolic acidosis starts at about 12 hours, after ingestion. Whereas before that time, there is a respiratory alkalosis. Since the question states 3 hours after ingestion, this could make choice C correct right?
No, C implies a metabolic alkalosis. That would not occur as a compensation to respiratory alkalosis or from any primary response to ASA overdose.
Frankly, I don’t think a strict time course cutoff question is the most likely test question people are going to get. By all means memorize the 12-hour “cutoff” (though it’s not a cutoff in real life; it’s more like a continuum between “early” and “late”).
But C is internally inconsistent. The only answer choice that can possibly be correct in this scenario is B.
Hey Ben, i took this practice session at the center.There were a total of 120 questions. I believe the three missing contained media. Any chance you came upon them? One was a murmur question of a child who had a tonsillectomy done years ago with a recurrent otitis media, with a stethoscope. Another was a primitive reflex with a video of the baby. Thanks for your help.
Never mind. I was able to access them by actually launching the program based questions. But yes, three media questions that are not included in the normal pdf. So I suggest all to attempt these sample questions through the program to simulate the exam to the fullest. Thanks
There have been a few multimedia questions on every set for the past few years in the software version.
In the past, I’ve always done the PDF version because the software was only available for Windows machines. Now that it is browser-based, I’m tempted to switch over, but I probably won’t, because using the PDF versions allows me to make relatively quick comparisons between the new and old sets for repeats etc.
Firstly, this is awesome. Secondly, why isn’t the answer to question 43 “EBV”? Isn’t EBV related to CNS Lymphoma. I assumed that her IgG Toxoplasmosis antibodies were telling you that Toxo was not the answer.
Thanks. Few reasons:
1. Remember CNS toxoplasmosis in HIV patients is a reactivation illness. So prior exposure is typical, not protective. Contrast this with what you were thinking, which applies to pregnant patients. Only new exposure to toxo during pregnancy can result in a TORCH infection, so having a positive IgG is “protective.”
2. EBV antibodies not mentioned. While also highly associated with CNS lymphoma, it would be less correct to say EBV infection causes CNS lymphoma (certainly compared to saying toxoplasma infection causes toxoplasmosis).
3. Multiple lesions favors toxoplasma over lymphoma. So does acute onset + fever. B-symptoms in lymphoma are usually of the low-grade fever + night sweats variety and do not typically occur in primary CNS lymphoma.
I tought nitroglycerin wpuld increase heart by ddcrease blood prwssure and beta blocker decrease blood pressure causing no change? Little confused about that :/
Someone asked a similar question higher up, see that discussion.
thank you very much :) I guess i have to read the question really well before answering, i notice that I make a lot of stupid mistakes and its not that i dont know the concept. its more about the question and what i understand they are asking.
I was wondering. I got in the prometric center a 78% yesterday taking this exam, what does that correlate in the real deal? i got 26 questions wrong from 120 questions
See this post about score correlations.
Also wanted to ask, i got a 220 in nbme 17, 78% prometric center and 239 in uworld assessment 1, im going to do nbme 19 this week too but i have two more weeks, my exam is april 7. what u think i should do these last two weeks? today i focused in all the questions of all the free questions in this website doing them and then looking at explanations but now for example im going to start studying because i finished anything, i was thinking to do first aid and pathoma but i dont know if these two last week si should or i should just do questions; what u think is better, i really want to go up, i want so badly a 230 its not even funny
I’d do questions during the final push. Simulating large blocks (like doing three blocks in a row before reviewing) can also be helpful for building up your stamina for the big day. Make sure to take the time to sleep and eat well starting now.
Thanks so much for taking the time to put all these together, this is a great resource!
Just a quick correction:
Block 1, Q39
mab stands for Monoclonal Anti-Body, not mouse antibody. You can tell if a monoclonal antibody (-mab) is mouse derived if the middle of the word contains -o-; I don’t think many of these are used anymore (can’t find a quick example), as they probably generate a significant immune reaction.
If the middle contains -xi-, it is a chimeric antibody (human Fc region, mouse variable region), such as infli-XI-mab; if the middle contains -zu-, it is a humanized antibody (only the antigen recognition site is foreign), such as adali-ZU-mab. I guess those small foreign parts can still generate an immune response.
Nice catch, thanks!
Thanks very much for taking the time to put this together. Excellent resource.
One minor point regarding Block 1 Question 40 – I believe H. pylori is able to increase the pH of its local environment (rather than decrease as you currently have written) allowing it to survive in the otherwise acidic gastric environment. This is achieved via ammonia production as you mentioned.
Absolutely. Good catch on the slip. And to think I always wondered why there were so many First Aid errata back in the day.
These explanations are so baws. Thanks! Just had my 150 yesterday and now I can see what I did wrong/right. You da boss man.
for question 81, the PTT is normal, doesn’t that rule out von Willebran disease? I thought afibrinoginemia would be the right answer since it would fit all the labs since platelets, PT, and PTT are all normal.
You’re overthinking it. While PTT is mildly elevated in about 50% of people, it is also commonly normal (and is more commonly often given as normal on tests). The classic boards scenario is normal PTT, normal PT, and elevated bleeding time.
How come the platelet aggregation studies are normal? Is this different from ristocetin cofactor assay?
Related but different. The cofactor assay uses patient’s plasma but not their own platelets.
Regardless, people overthink this question. There are multiple VWD types with type 1 being a relative quantitative deficiency, which often has normal laboratory studies. This may be of interest:
Thank you for the explanation. One question: In Block 1, question 17. Wouldn’t timolol (non-specific beta 1 & 2 blocker) inhibit the actions of Albuterol (inhaled short-acting beta2-agonist) since it’s occupying the beta 2 receptor?
Sure they can compete, doesn’t change the answer though and doesn’t mean albuterol will have no effect.
Hi! thank you so much for putting this together, its incredibly helpful.
I had a question about 44- at what point would the kidneys go from conserving water to acute tubular necrosis? Do we just assume that they kidney function is fine even though it appears there has been a significant loss of blood?
Well you know they’re going to be conserving water until they fail, so I don’t think it would be ever be a good idea to jump the gun to ATN until you have objective evidence of renal failure and not just a prerenal state.
Ben hi, thanks so much for this wonderful resource and all the time you’ve put into it. Actually for the whole site in general, especially as someone also interested in radiology, I’ve found your site very useful time and time again in med school.
This is quite some time after the original post and I’m sure you’re quite busy, but if you ever had the time it’d be great if you could write your short explanations for the final three questions of block 3 which are left out above.
Two are quite tricky; I’m having a hard time understanding what I can take away from them in order not to get such things wrong in the future, because very little context is given for why these exams are ‘normal’:
38 is a cardiac ausculation question where there appears to be an extra sound every few beats, and the indicated correct answer is “Normal findings”.
39 is a neonatal reflex examination with a video clip, that looks unusual but the correct answer is also “Normal findings”.
(40 is a video clip question that very obviously shows Parkinsons and the answer to is “substantia nigra”, so very straightforward.)
Either way, again thanks so much!
For context: on 39 my wrong answer was ‘Tay-Sachs’ (hyperreflexia being a symptom), don’t remember exactly which ‘wrong answer’ for 38 cardiac question.
I addressed them in a separate post, but I never went back and added them to this one. Here: https://www.benwhite.com/medicine/explanations-for-the-2017-official-step-1-practice-questions/.
Thanks so much for this. I was wondering if you could explain why the man in #7 in Block 1 (the shock question) has decreased O2 saturation in his veins if he’s just hypovolemic? Wouldn’t the O2 saturation be normal since all the RBCs he has are fully saturated (even if he has fewer of them since he’s losing blood)…? I think I’m just confused. Thank you!
Central venous O2 saturation is not just a function of the individual efficiency of individual RBCs. From a random paper:
it’s a reflection on of tissue oxygenation, which is a combination of blood oxygenation, perfusion, and oxygen extraction. It’s commonly used in the setting of shock, as redistribution/shunting of blood causes the decrease. This is felt to be more clinically meaningful than simple pressure measurements, though of course the latter is also always used in conjunction.
Sorry for the double post but I have another question if you don’t mind. For #95, how do you know it’s a B12 deficiency and not a B1 deficiency (dry beriberi)? I saw a Uworld question that was similar (old person w/ peripheral neuropathy) and it was B1…
Random link: http://neuropathology-web.org/chapter8/chapter8Nutritional.html
Note that SCD is in the cord and results in spastic paralysis. Berberi affects peripheral nerves.
Any question is most likely to hinge on contributing history or other factors. Old person person living alone (tea and toast diet), strict vegetarians, macrocytic anemia, findings suggestive of pernicious anemia symptoms – B12. Alcoholic or homeless, other signs of WKS, ophthalmoplegia, etc – B1.
Ah, I see. Thank you so much for the fast response, and thanks so much for putting these great answer keys together, I don’t know how I would understand some of these questions without your explanations!
Thank you so much Ben! Currently 2 days out from my test and really glad I found your site just in the nick of time.
Question about Block 3, #96: The patient has AML and granulocytopenia. I chose that she would be predisposed to dimorphic fungi (I was thinking Candida). Would you just not choose that because bacteria is more likely, or why not?
Also- do you have any last minute advice on how to avoid overthinking / silly mistakes? I know it’ll be inevitable that there will be a few, but I’d like to hear if you had any advice or tips on minimizing them. Thank you!
Remember to read the actual question wording carefully. It’s not: what is an immunocompromised person at risk for? It is: what kind of infection does granulocytopenia (essentially neutropenia) predispose to? Which is also getting at a core microbio concept: what is the primary function of neutrophils? The answer is to fight bacterial infection.
In contrast, fungal disease is primarily combatted via cell-mediated immunity. This is why thrush is seen in AIDS with low cd4 counts.
I touch on some of that overthinking/anxiety at the bottom of this post.
Overthinking a question is a symptom of underconfidence. You overthink and question yourself because you believe that you are insufficiently prepared to determine which facts are pertinent to picking the correct answer. Therefore you start searching hidden clues to avoid making a “silly” mistake. The only solution to me is to believe that you are as prepared as you can reasonably be and that you should use the skills you have to answer to the best of your actual ability.
thank you. In ques 55 should’nt it be alpha value instead of p value in your explanation?
Yeah. The alpha is the threshold for which a p-value is deemed significant.
Thank you for answering questions even a year after you made this!
I have a question for #92 – the patient with intermittent asthma and a cough. Due to his 1 week history of cough/malaise and clear sputum, and normal current RR, I thought Dextromethorphan would be used just to treat the cough. Why would you use albuterol to treat the cough? Perhaps if a patient has untreated asthma and they present with anything related to it you would just start albuterol..
Also, when would you use Guaifenesin? If there was a lot of mucus but no signs of bacterial infection?
The patient has wheezing, which is related to his asthma. Cough is also a very common symptom of asthma (in some cases, it is the only symptom of asthma, which is sometimes referred to as cough-variant asthma).
While there may be some underlying viral cause of the current exacerbation, both cough and wheezing are a convincing pair for at least a large component of reversible airway disease, which is best treated in the acute setting with albuterol.
Dextromethorphan may alleviate cough symptoms but will do nothing for asthma-related cough. As a practical matter, somebody with underlying asthma will pretty much always need a beta agonist in the setting of any respiratory problems.
Guafenesin will probably never be the correct answer. Frankly, it doesn’t actually do much. Generally, symptomatic treatments are less commonly tested than treatments for actual disease processes.
94. Although answer D is correct, name for the migrating serpiginous pruritic perianal rash is cutaneous larva migrans, a condition caused by Ancylostoma duodenale and Necator americanus. They aren’t caused by Strongyloides.
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 eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil). Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason.
thank you so much for these amazing explanations.
For 65 – I chose Degranulation of eosinophils because i thought it was some kind of hypersensitivity reaction. I am very confused on this topic because whenever I see edema, red, itchy I automatically think of IgE degranulation. Can you explain to me how the scenario in this question is different?
Time course and exam are wrong for that.
IgE should make you think of hives. Happens essentially immediately, erythematous edematous wheal/plaque.
This case is a fluctuant area two *days* later. Fluctuant means pus/abscess.
Ahhh i see. thank you so much!
Question 86: Don’t fungal infections induce a T-helper response specifically a TH1 subset that produces IFN-gamma to clear fungal infections? TH2 subset (Immunoglobulins and Eosinophils) for bacteria and parasitic infections?
I meant question 83
for question B
how can I know if it’s early or late aspirin toxicity
-I remember doing Q bank X and they wrote there speficially that concomitant metabolic acidosis begin after 12 hours or so.
meant to say 38
This was discussed a couple separate times in the comments above
about question 37
Is there a situation in which a patient wants to date a doctor(e.g. GP) and it is allowed, as in “after 2 years” or so?
There is not a specific time frame. Practically, sure, that’s probably fine. But I wouldn’t go for the bait if it appeared on a test.
Thank you! a lot!
About Question 107:
-In the picture you also see Target cells > suppose to be in case of nonfunctioning spleen in sickle cell, so how can his LUQ be d/t the spleen?
-Do we see also Spherocytes in the pictures? and if yes, can you please explain why?
-His platelet count is also low, why would that be?
Thank you very very much for you awesome job!
Are these sample questions and fred test same or different????
Same but in different order (and the online one includes a few multimedia ones).
Great job Ben! Thank you for putting this together and helping myself and so many other students prepare for their STEP 1 exam.
My one question is for the #43 “so easy it defies logic” question (I got it wrong, lol). You are right, all signs were pointing to either Toxo or CNS lymphoma, however I refused to choose Toxo, because the question states that there are Anti-Toxo IgG antibodies present in the patients serum. Therefore I assumed that the question was telling me that there is no way the patient has Toxo, because she is protected by antibodies… What am I doing wrong here?
Okay, I just read that you have already answered this question in a previous post. Thank you.
Hi Ben! Thank you so much for your explanations!
PS: I have tried to find the PDF of that exam, but I was not able to do so. The one that is on the official web page is the “new version”. Do you happen to have a copy of the questions you posted?
The link posted at the top of the page is to the archive.org cached version of the PDF, since the original link is no longer active.
Yes! Had some “internet security issues” with the link, but I got the PDF at the end. Thanks!
Yes, some browsers, particularly chrome, are getting really picky about the SSL certificate details on secure (https) sites.
thank u so much for the explanation and the effort.
my query is for Q #17.
albuterol is a standard emergency treatment for bronchodialtion,
in glaucoma patient it applies same? as timolol is removed and beta agonist given.
what will happen to glaucoma?
Presumably, the glaucoma will be temporarily less well-treated, but we’re talking acute problems trumping chronic problems. Regardless, someone with asthma should be on a different glaucoma med.