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Why the Praxler Q-Bank feels different.
Built to mirror real exam pressure and depth — with explanations that go beyond “the answer is C” and actually teach you the mechanism.
4,000+ hand-crafted questions
Long-form clinical vignettes matched to the difficulty and style of real USMLE & PLAB exams — covering all high-yield systems, subjects and organ blocks.
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Every explanation walks through the molecular and pathophysiologic “why” behind the right and wrong options — perfect if you want to actually understand, not memorise.
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Realistic vignettes, clear answer choices, and explanations that walk you through the underlying physiology and pathology — just like you asked for.
A 58-year-old man presents with sudden-onset severe chest pain that began 40 minutes ago while climbing stairs. The pain radiates to his left arm and jaw and is associated with diaphoresis and nausea. He has a history of hypertension and hyperlipidaemia and smokes 20 cigarettes per day.
Blood pressure is 92/58 mmHg, pulse is 110/min, and respiratory rate is 22/min. Examination reveals cool extremities and elevated jugular venous pressure. ECG shows ST-segment elevation in leads II, III, and aVF.
Which of the following best explains the mechanism underlying his hypotension?
ST elevation in II, III, and aVF indicates an inferior-wall myocardial infarction, most commonly due to occlusion of the right coronary artery. In many patients, the right ventricle is also affected.
The right ventricle is responsible for delivering blood to the pulmonary circulation, which then returns to the left atrium and left ventricle. In a right ventricular infarct:
- Right ventricular contractility falls → right ventricular output decreases.
- Less blood reaches the pulmonary circulation → reduced left ventricular preload.
- Lower preload → reduced stroke volume and cardiac output → hypotension.
Elevated JVP and hypotension with clear lungs are classic for a right ventricular MI: the failing right ventricle backs blood up into the systemic venous system, while the left side is underfilled.
Why the others are wrong:
- A: Loss of sympathetic tone describes neurogenic shock (e.g. high spinal cord injury), not acute inferior MI with ST elevation.
- B: LV outflow obstruction (e.g. severe aortic stenosis, HOCM) would give a harsh systolic murmur and chronic symptoms, not acute inferior ST elevations.
- D: Acute aortic regurgitation causes sudden volume overload and pulmonary oedema with a diastolic murmur, not isolated JVP elevation with clear lungs.
- E: Massive PE causes acute right heart strain and hypoxia, but ECG would not show classic inferior ST elevations.
A 32-year-old woman presents with weight loss despite increased appetite, heat intolerance, and palpitations. She reports difficulty sleeping and increased anxiety. On examination, she has a fine tremor, warm moist skin, and a diffusely enlarged nontender thyroid gland.
Laboratory studies show suppressed TSH and markedly elevated free T4. Thyroid-stimulating immunoglobulins are present.
Which of the following best describes the primary mechanism driving her symptoms?
The patient has classic Graves disease: diffuse goitre, ophthalmic symptoms may develop, and labs show low TSH with high free T4 plus thyroid-stimulating immunoglobulins.
In Graves, IgG autoantibodies bind to and activate the TSH receptor on thyroid follicular cells. The TSH receptor is coupled to a Gs-protein, which:
- Increases adenylyl cyclase activity → ↑ cAMP
- ↑ Synthesis and release of T3/T4
- Stimulates follicular cell growth → diffuse goitre
The resulting excess thyroid hormone increases basal metabolic rate (via upregulation of Na+/K+-ATPase) and β1-adrenergic receptor expression, explaining tachycardia, tremor, heat intolerance, and weight loss.
Why the others are wrong:
- B: Describes subacute or painless thyroiditis — would cause a transient thyrotoxic phase without a sustained stimulatory antibody.
- C: Impaired T4→T3 conversion would reduce active hormone, tending towards hypothyroid features.
- D: Blocking TPO would reduce hormone synthesis → hypothyroidism (e.g. Hashimoto), not Graves hyperthyroidism.
- E: An activating nuclear receptor mutation is not the usual mechanism in common hyperthyroidism and would not explain a diffuse goitre driven by TSH receptor activation.
A 24-year-old man with a history of asthma presents with worsening shortness of breath and wheeze after exposure to cold air. He uses his short-acting β2-agonist inhaler several times per week.
Spirometry performed between attacks shows:
FEV1: 70% predicted (improves to 90% after bronchodilator)
FVC: 95% predicted
FEV1/FVC ratio: 0.65 (normal ≥ 0.75)
Which of the following best explains the change seen after administration of the β2-agonist?
The reduced FEV1 with relatively preserved FVC and low FEV1/FVC ratio are typical of obstructive lung disease. The large improvement in FEV1 after bronchodilator is characteristic of asthma.
Short-acting β2-agonists (e.g. salbutamol) bind to β2 receptors on bronchial smooth muscle. These are Gs-coupled receptors that:
- Activate adenylyl cyclase → ↑ cAMP
- Activate PKA → phosphorylation of targets that ↓ intracellular Ca2+
- Result in smooth muscle relaxation → bronchodilation
Bronchodilation decreases airway resistance, so more air can be exhaled in the first second, increasing FEV1 and improving the FEV1/FVC ratio.
Why the others are wrong:
- A: Airway wall compliance is not the main target of β2-agonists; they mainly relax smooth muscle.
- C: Increased mucus worsens obstruction and would lower FEV1 further.
- D: Irreversible remodelling describes chronic COPD changes, which are poorly reversible with bronchodilators.
- E: M3 blockade is the mechanism of antimuscarinic agents (e.g. ipratropium), not β2-agonists.
Designed for IMGs who want more than a question dump.
Classic Q-banks test you. Praxler Q-Bank teaches you while it tests you — so your understanding compounds every time you log in.
What you get inside Praxler Q-Bank
- Realistic, exam-length clinical vignettes with multi-step reasoning.
- Mechanism-heavy explanations that link each question back to First Principles.
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- Adaptive blocks that keep returning to your blind spots until they’re gone.
- Effortless tracking across systems, subjects, exam objectives and NBME-style categories.
Typical Q-banks
- Random, mixed-quality questions from multiple sources.
- “The answer is C because…” explanations that don’t deepen understanding.
- No real sense of where you sit compared with other serious candidates.
- Weak analytics that tell you only how many questions you’ve done.
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Questions about Praxler Q-Bank, answered.
A focused tool for ambitious candidates. Here’s what most people ask before they join.