United States Medical Licensing Examination Step 1

Basic and mechanistic science applied to clinical vignettes. Reported pass/fail since 2022, which changed how candidates should allocate time but not how hard it is.

United StatesNBME / FSMB written

Coming soon. This bank is still in build and not on sale yet. The banks live now are PLAB 1, MRCP Part 1 and AMC MCQ.

What is on the USMLE Step 1?

Questions or stations	280 verified 2026-08-10 Source says: “a total of up to 280 items on the examination” check it yourself
Time	480 minutes verified 2026-08-10 Source says: “administered in one 8-hour testing session” check it yourself
Format	Single best answer vignettes in timed blocks
Adaptive delivery	No
Pass mark	Reported as pass/fail. The underlying standard is set by the USMLE programme and reviewed periodically. verified 2026-08-10 check it yourself
Blueprint	USMLE Content Outline and Specifications, NBME / FSMB

Up to 280 items across the day's blocks in one 8-hour session; reported as pass/fail, not a three-digit score.

Verification status. All 3 published figures on this page have been read in the source document and dated above. Source of truth: USMLE Content Outline and Specifications, NBME / FSMB. How we verify.

The USMLE Step 1 curriculum, section by section

Every question in this bank is tagged to one of the sections below, and the tag traces to USMLE Content Outline and Specifications. That is what makes a coverage claim checkable instead of a marketing line. The table shows exactly how many items exist in each section today, including the sections where the answer is none.

Curriculum section	Share of the blueprint	Items in this bank
Pathology and pathophysiology	22%	10
Physiology	16%	6
Pharmacology	12%	6
Biochemistry and nutrition	11%	4
Microbiology	10%	5
Gross anatomy and embryology	7%	3
Immunology	6%	3
Histology and cell biology	5%	3
Behavioural sciences	5%	1
Genetics	4%	2
Biostatistics and epidemiology	2%	3

Coverage today: 11 of 11 sections. We publish the gap rather than hiding it.

Free sample questions

Full explanations for every option, including the ones you didn't pick. The option you nearly chose is usually the one you needed explained. Read these before paying for anything.

A 6-month-old infant presents with hepatomegaly, hypoglycemia after short fasts, lactic acidosis, hyperuricemia and hyperlipidemia. Muscle strength is normal. Liver biopsy shows markedly increased glycogen with normal structure. Which enzyme is most likely deficient?

Glucose-6-phosphatase correct Correct. This is Von Gierke disease (type I). Glucose-6-phosphatase is the enzyme the liver needs to release free glucose, whether from breaking down glycogen (glycogenolysis) or from building new glucose (gluconeogenesis). Without it, the liver cannot release glucose at all, so fasting hypoglycemia starts early and is severe. The blocked pathway pushes extra substrate toward lactate, uric acid, and triglycerides.
Branching enzyme Wrong. Missing branching enzyme causes Andersen disease, with liver scarring (cirrhosis) and failure to thrive from abnormally branched glycogen. The biopsy here shows glycogen with a normal structure, which rules this out.
Muscle glycogen phosphorylase Wrong. Missing this enzyme causes McArdle disease, which affects only the muscles: exercise intolerance, cramps, muscle breakdown that shows up as myoglobin in the urine (myoglobinuria), and lactate that fails to rise with exercise. The liver and blood glucose stay normal.
Debranching enzyme Wrong. Missing this enzyme causes Cori disease (type III), which gives milder fasting hypoglycemia, glycogen with an abnormal structure, and normal lactate, because gluconeogenesis still works.
Lysosomal acid alpha-1,4-glucosidase Wrong. This enzyme is missing in Pompe disease, which enlarges the heart (cardiomegaly), causes floppy muscles (hypotonia), and leads to early death. Blood glucose stays normal in Pompe disease because the cell's normal way of using glycogen, outside the lysosome, still works.

The point: Sort the glycogen storage diseases by which organ is affected and whether lactate rises. Type I (Von Gierke): liver, severe fasting hypoglycemia, HIGH lactate. Type III (Cori): milder, normal lactate. Type V (McArdle): muscle only. Type II (Pompe): heart.

Source: USMLE Content Outline — biochemistry and nutrition NBME / FSMB (USMLE programme) · tier 0, exam blueprint / regulator

A 58-year-old man is started on a new antihypertensive. Two weeks later he develops a dry, persistent cough. Serum potassium has risen from 4.1 to 5.2 mEq/L and creatinine from 0.9 to 1.1 mg/dL. Which mediator most directly explains his cough?

Histamine Wrong. Histamine drives immediate allergic reactions, hives (urticaria), airway tightening (bronchospasm), and flushing. It does not cause the delayed dry cough seen with ACE inhibitors.
Prostaglandin E2 Wrong. Prostaglandin E2 may sensitize the airway in some lab models, but the mediator that builds up directly because of ACE inhibition is bradykinin. Switching to an ARB (angiotensin receptor blocker) fixes the cough exactly because ARBs do not change how bradykinin is broken down.
Aldosterone Wrong. Aldosterone is also reduced by the drug, which is why potassium went up. Aldosterone plays no part in triggering a cough.
Angiotensin II Wrong. The drug lowers angiotensin II, it does not raise it. This drop in angiotensin II explains the fall in blood pressure and the rise in potassium, but not the cough.
Bradykinin correct Correct. ACE (also called kininase II) breaks down bradykinin, on top of its main job of turning angiotensin I into angiotensin II. Blocking ACE lets bradykinin and substance P build up in the airway. This causes the dry cough seen in roughly 5 to 20% of patients, and rarely, swelling of the face or throat (angioedema).

The point: ACE inhibitor cough and angioedema (swelling) are caused by too much bradykinin. The rise in potassium (hyperkalemia) and creatinine happens because of lower angiotensin II, a separate, expected effect of the drug. Switching to an ARB fixes the cough, but the potassium effect stays, because that effect is part of how the drug class is meant to work.

Source: USMLE Content Outline — pharmacology NBME / FSMB (USMLE programme) · tier 0, exam blueprint / regulator

Where USMLE Step 1 sits in the pathway

US licensing (USMLE) runs USMLE Step 1 → USMLE Step 2 CK → USMLE Step 3. One DocPasser account covers all of them, so moving to the next stage does not mean a new account and a progress history you can no longer see.

USMLE Step 2 CK · USMLE Step 3

Questions people actually ask about USMLE Step 1

Is USMLE Step 1 pass/fail?

Yes — results have been reported as pass or fail since January 2022. Residency programmes responded by leaning harder on Step 2 CK, so treating Step 1 as a formality is a mistake with a delayed cost.

How many questions are on Step 1?

The test day is built from timed blocks with an upper bound on total items. Confirm the current block structure against the USMLE website for your test year.

What does USMLE Step 1 preparation cost?

USMLE Step 1 is a flat £20 for 12 months of access — one price, one purchase, no tiers. The first 10 questions are free, with the full explanation for every option, so you can judge the quality of the explanations before paying for anything.