ABOHNS Qualifying Exam Prep & OTE Study Questions

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ABOHNS Written Boards (Written Qualifying Examination / WQE) question bank, mock exams, and analytics by OtoPrep.

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A 24-year-old man is brought to the emergency department after a high-speed motor vehicle collision. He is intubated for airway protection. On facial examination, there is marked midface flattening, bilateral periorbital ecchymosis, and telecanthus. When the maxilla and nasal bridge are grasped, the entire midface, including the zygomas, moves as a single unit relative to the cranial vault.

Maxillofacial CT shows bilateral fractures extending through the nasofrontal suture, the frontal process of the maxilla, the ethmoid sinus and lamina papyracea, the orbital floors to the region of the inferior orbital fissures, and then laterally through the zygomaticofrontal sutures and zygomatic arches, with involvement of the pterygoid plates.

Which ONE of the following fracture patterns best describes this injury?

Horizontal maxillary fracture passing above the tooth roots, through the maxillary sinuses and pterygoid plates, sparing the nasal bones and orbits

Isolated zygomaticomaxillary complex fracture involving the zygomatic arch, lateral orbital wall, and zygomaticomaxillary buttress with intact nasofrontal suture and pterygoid plates

Isolated naso-orbital-ethmoid fracture involving the nasal bones, medial orbital walls, and frontal process of the maxilla without separation of the zygomatic arches from the cranial base

Craniofacial disjunction with fracture lines through the nasofrontal suture, medial and lateral orbital walls, orbital floors to the inferior orbital fissures, zygomaticofrontal sutures, zygomatic arches, and pterygoid plates

Pyramidal fracture extending from the maxillary alveolus through the inferior orbital rims and nasal bones to the nasofrontal region, with pterygoid plate involvement but intact zygomatic arches

Tutor-style explanation

Correct answer: D.

Explanation:
Why this option is correct:
The described CT findings show a high-level midface fracture pattern in which the entire midface is separated from the cranial base. The fracture traverses the nasofrontal suture, the frontal process of the maxilla, the ethmoid sinus and lamina papyracea, the orbital floors to the inferior orbital fissures, and then extends laterally through the zygomaticofrontal sutures, zygomatic arches, and pterygoid plates. This constellation defines a Le Fort III fracture, also known as craniofacial disjunction, in which the midface skeleton is dissociated from the frontal bone and anterior cranial base.

Why the other options are wrong:
The description of a horizontal maxillary fracture passing above the tooth roots through the maxillary sinuses and pterygoid plates, while sparing the nasal bones and orbits, corresponds to a Le Fort I pattern. Le Fort I fractures do not involve the nasofrontal suture, lamina papyracea, orbital floors, or zygomatic arches and therefore do not produce complete craniofacial separation as in this case.

The pyramidal fracture passing from the alveolus through the inferior orbital rims and nasal bones up to the nasofrontal region, with pterygoid plate involvement but intact zygomatic arches, describes a Le Fort II injury. Le Fort II fractures typically involve the inferior orbital rims and nasal bones but do not extend laterally through the zygomaticofrontal sutures or zygomatic arches, which are key features of a Le Fort III craniofacial disjunction.

An isolated zygomaticomaxillary complex fracture involves the zygomatic arch, lateral orbital wall, and zygomaticomaxillary buttress, but by definition spares the nasofrontal suture, medial orbital walls, and pterygoid plates. While zygomaticomaxillary complex injuries can cause significant deformity, they do not result in the entire midface moving as a unit relative to the cranial vault and therefore are not classified as Le Fort III fractures.

An isolated naso-orbital-ethmoid fracture affects the nasal bones, medial orbital walls, and frontal process of the maxilla, with potential telecanthus, but does not include separation of the zygomatic arches and lateral orbital walls from the cranial base. Without involvement of the zygomaticofrontal sutures and zygomatic arches or global midface mobility, this pattern cannot be considered a Le Fort III craniofacial disjunction.

Further Reading:
Zimmerer RM, et al. Midface fractures I: Le Fort fracture patterns and their management. Head Face Med. 2017 (PMC)
Sturdza A, et al. Facial fractures: classification and highlights for a useful report. Insights Imaging. 2020 (PMC)
Strong EB. Maxillofacial trauma. In: Cummings Otolaryngology – Head and Neck Surgery. 6th ed. (EntoKey)

Additional Concepts:
• All classic Le Fort fractures involve the pterygoid plates; absence of pterygoid plate fractures on CT should prompt reconsideration of the diagnosis and alternative fracture classifications.
• Le Fort II and III fractures are often part of complex panfacial injury patterns that may coexist with naso-orbital-ethmoid fractures, zygomaticomaxillary complex fractures, and cranial base injuries, requiring careful CT review and multidisciplinary management.
• Clinically, Le Fort III injuries can present with marked midface retrusion, lengthening of the face, malocclusion, telecanthus, and mobility of the entire midface in relation to the cranial vault when stressed manually.
• Definitive management of Le Fort III fractures focuses on restoring the facial skeletal buttresses and occlusion, typically using open reduction and rigid internal fixation anchored to stable cranial and frontal bone segments, often via coronal and intraoral approaches.

A clinician is triaging referrals for patients with persistent hoarseness. All have had symptoms for 6 weeks without improvement despite conservative management. Limited clinic capacity means that only ONE patient can be prioritized for same-week laryngoscopy.

Based on typical epidemiologic risk factors for laryngeal cancer, including age, sex, and tobacco exposure, which ONE of the following patients is at HIGHEST risk for underlying laryngeal cancer and should be prioritized?

A 65-year-old woman who has never smoked but has long-standing gastroesophageal reflux disease

A 35-year-old man with a 10 pack-year smoking history who quit 5 years ago

A 30-year-old male teacher with heavy voice use but no history of smoking or alcohol abuse

A 50-year-old woman with heavy alcohol use and reflux symptoms but no tobacco exposure

A 65-year-old man with a 40 pack-year smoking history who currently smokes one pack per day

Tutor-style explanation

Correct answer: E.

Explanation:
Why this option is correct:
The 65-year-old man who is a current heavy smoker fits the classic high-risk demographic for laryngeal cancer: male sex, age over 40–50 years, and substantial ongoing tobacco exposure. Tobacco smoking is the dominant risk factor for laryngeal squamous cell carcinoma, and risk increases with cumulative pack-years and persists with continued use. In a patient with persistent dysphonia, this profile confers the highest pretest probability of laryngeal cancer and warrants expedited laryngoscopic evaluation.

Why the other options are wrong:
The older woman with no smoking history but gastroesophageal reflux disease has some risk from reflux-related mucosal irritation, but in the absence of tobacco exposure her overall risk for laryngeal cancer is significantly lower than that of an age-matched male smoker. She still merits evaluation but is not the highest priority in this group.

The younger man with a modest 10 pack-year history who quit smoking 5 years ago carries some increased risk compared with a never-smoker, but his younger age and relatively limited tobacco exposure place him at lower risk than a 65-year-old current heavy smoker with persistent symptoms.

The 50-year-old woman with heavy alcohol use and reflux but no tobacco exposure has elevated risk from alcohol, but alcohol acts synergistically with tobacco; in isolation, its effect is weaker than tobacco’s. Without smoking, her demographic risk for laryngeal cancer is lower than that of the older male current smoker.

The 30-year-old male teacher with heavy voice use and no major carcinogenic exposures is more likely to have benign voice disorders such as muscle tension dysphonia, nodules, or polyps. While persistent hoarseness still requires evaluation, his demographic risk for laryngeal cancer is the lowest among the listed patients.

Further Reading:
Marur S, Forastiere AA. Laryngeal Cancer. StatPearls. Treasure Island (FL): StatPearls Publishing; 2024. [NCBI Bookshelf]
Zhang L et al. Global trends and risk factors of laryngeal cancer: a systematic analysis for the Global Burden of Disease Study 1990–2021. BMC Cancer. 2025;25:13700.
Bosetti C et al. Laryngeal cancer in women: tobacco, alcohol, nutritional, and hormonal factors. Br J Cancer. 2003;88(5):815-819.

Additional Concepts:
• Tobacco use is the single most important modifiable risk factor for laryngeal cancer, with risk increasing dose-dependently with pack-years and remaining elevated for years after cessation, though it gradually declines over time.
• Historically, laryngeal cancer has one of the highest male-to-female incidence ratios among solid tumors, reflecting historically higher smoking and heavy alcohol consumption rates in men, though this gap is narrowing as smoking patterns change.
• Human papillomavirus is strongly implicated in oropharyngeal carcinoma but plays a more limited and less well-established role in laryngeal carcinogenesis compared with tobacco and alcohol exposure.
• Occupational exposures such as asbestos, wood dust, paint fumes, and certain industrial chemicals can modestly increase the risk of laryngeal cancer, particularly when combined with tobacco and alcohol, and should be considered when taking a detailed occupational history.

A 39-year-old woman presents with several months of progressive diplopia and right-sided headache. MRI demonstrates a lobulated, T2-hyperintense, enhancing mass centered on the right petroclival junction, eccentrically located off the midline, with characteristic "ring-and-arc" calcifications on CT. Biopsy confirms a low-grade skull base chondrosarcoma. From which ONE of the following structures does this tumor most typically arise?

Schwann cells of the vestibulocochlear nerve in the internal auditory canal

Meningothelial (arachnoid cap) cells along the dura

Residual chondrocytes within the petroclival synchondrosis of the skull base

Notochordal remnants within the midline clivus

Epithelial remnants of Rathke pouch in the sellar region

Tutor-style explanation

Correct answer: C.

Explanation:
Why this option is correct:
Skull base chondrosarcomas are mesenchymal malignancies with cartilaginous differentiation that arise from residual chondrocytes within the endochondral synchondroses of the skull base, most commonly the petroclival synchondrosis at the junction of the clivus and petrous temporal bone. This cartilaginous joint persists as a plate of hyaline cartilage in adult life and provides the cartilage-forming cell population that can undergo malignant transformation, explaining the typical paramedian petroclival location of these tumors on imaging. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/9504309/?utm_source=otoprep))

Why the other options are wrong:
Notochordal remnants within the midline clivus give rise to chordomas, not skull base chondrosarcomas. Chordomas tend to be strictly midline, show physaliphorous cells histologically, and express cytokeratin and brachyury, whereas chondrosarcomas are usually lateral to the midline at the petroclival synchondrosis and lack brachyury expression.

Meningothelial arachnoid cap cells are the cell of origin for meningiomas. These tumors are typically dural-based, extra-axial masses with a broad dural attachment; when they occur near the skull base they may mimic chondrosarcoma radiologically but they do not originate in the petroclival synchondrosis or within bone.

Schwann cells of the vestibulocochlear nerve give rise to vestibular schwannomas (acoustic neuromas). These lesions typically center on the internal auditory canal and cerebellopontine angle, enhance homogeneously, and remodel the porus acusticus; they do not show a chondroid matrix with ring-and-arc calcifications and are not derived from cartilaginous rests.

Epithelial remnants of Rathke pouch are the source of craniopharyngiomas, which arise in the sellar and suprasellar region. They frequently contain cysts and coarse calcifications and are not centered on the petroclival junction; they have an epithelial rather than cartilaginous origin.

Further Reading:
Ditzel Filho LFS, et al. The endoscopic endonasal approach for removal of petroclival chondrosarcomas. Neurosurg Clin N Am. 2015;26(3):453-462. [PubMed]
Oghalai JS, et al. Skull base chondrosarcoma originating from the petroclival junction. Otol Neurotol. 2005;26(5):1052-1060. [PubMed]

Additional Concepts:
• Chordomas and skull base chondrosarcomas can appear similar radiologically but usually differ in location: chordomas arise from notochordal remnants and are typically midline along the clivus, whereas chondrosarcomas more often arise paramedian from petroclival or other synchondroses.
• On imaging, skull base chondrosarcomas frequently show a lobulated contour with high T2 signal and characteristic ring-and-arc calcifications on CT, reflecting the hyaline cartilage matrix; recognizing this pattern helps distinguish them from meningioma and metastasis.
• Endoscopic endonasal approaches provide direct access to the petroclival synchondrosis, allowing resection of skull base chondrosarcomas with limited brain retraction; careful preoperative assessment of internal carotid artery course and cranial nerve anatomy is essential for safe surgery.
• Adjuvant high-dose conformal radiation, often using proton or carbon ion therapy, is commonly employed after subtotal resection of skull base chondrosarcomas to improve local control while limiting dose to adjacent cranial nerves and brainstem.

A 7-year-old boy presents with a rapidly enlarging mandibular mass and cervical lymphadenopathy. Biopsy confirms Burkitt lymphoma demonstrating a classic "starry-sky" appearance. Fluorescence in situ hybridization (FISH) is performed to identify the characteristic chromosomal abnormality. Which ONE of the following cytogenetic findings is MOST typical of Burkitt lymphoma?

Deletion of 13q14 involving RB1

t(11;14)(q13;q32) involving CCND1 and the immunoglobulin heavy-chain locus

t(9;22)(q34;q11) BCR-ABL1 fusion

t(8;14)(q24;q32) involving MYC and the immunoglobulin heavy-chain locus

t(14;18)(q32;q21) involving BCL2 and the immunoglobulin heavy-chain locus

Tutor-style explanation

Correct answer: D.

Explanation:
Why this option is correct:
The hallmark cytogenetic abnormality of Burkitt lymphoma is a translocation involving the MYC oncogene on chromosome 8 and an immunoglobulin locus, most commonly t(8;14)(q24;q32) involving the immunoglobulin heavy-chain locus on chromosome 14. This rearrangement leads to deregulated MYC expression, driving the extremely high proliferative rate characteristic of Burkitt lymphoma. Detecting a t(8;14) translocation supports the diagnosis and helps distinguish Burkitt lymphoma from other high-grade B-cell lymphomas in the head and neck region.

Why the other options are wrong:
The t(9;22)(q34;q11) BCR-ABL1 fusion is the defining chromosomal abnormality of chronic myeloid leukemia and is also found in a subset of acute lymphoblastic leukemias. It is not characteristic of Burkitt lymphoma and would suggest a different hematologic malignancy.

The t(11;14)(q13;q32) translocation involving CCND1 (cyclin D1) and the immunoglobulin heavy-chain locus is typical of mantle cell lymphoma, an adult-predominant lymphoma that rarely occurs in children and is not associated with the classic Burkitt morphology or clinical presentation seen in this vignette.

The t(14;18)(q32;q21) translocation involving BCL2 and the immunoglobulin heavy-chain locus is most commonly associated with follicular lymphoma and some diffuse large B-cell lymphomas. It leads to overexpression of BCL2 with inhibition of apoptosis, a mechanism distinct from MYC-driven proliferation in Burkitt lymphoma.

Deletion of 13q14 affecting RB1 is more commonly associated with certain leukemias and solid tumors but is not a defining or characteristic abnormality of Burkitt lymphoma. Its presence would not explain the classic pathologic and clinical features described in this case.

Further Reading:
Roschewski M, Wilson WH. Clinical manifestations, pathology, and diagnosis of Burkitt lymphoma. UpToDate
Molyneux EM et al. Burkitt's lymphoma. Lancet. 2012;379(9822):1234-1244.
Swerdlow SH et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood. 2016;127(20):2375-2390.

Additional Concepts:
• Besides t(8;14), variant Burkitt lymphoma translocations include t(2;8) and t(8;22), which juxtapose MYC to the immunoglobulin kappa or lambda light-chain loci. All of these rearrangements lead to MYC overexpression, underpinning the tumor's explosive growth and very high Ki-67 proliferation index.
• Endemic Burkitt lymphoma, common in certain regions of Africa, frequently presents with jaw or facial bone tumors and has a strong association with Epstein–Barr virus infection. Sporadic Burkitt lymphoma, more typical in North America, often presents with abdominal masses but can also involve head and neck sites.
• The "starry-sky" pattern on histology in Burkitt lymphoma reflects numerous tangible-body macrophages scattered among a uniform population of medium-sized neoplastic B cells. While suggestive, this pattern is not entirely specific and must be interpreted alongside immunophenotype and cytogenetic findings.
• Because of Burkitt lymphoma's high proliferation rate and chemosensitivity, prompt initiation of intensive combination chemotherapy can achieve excellent cure rates in children. However, the same biology confers a high risk for tumor lysis syndrome, necessitating meticulous peri-treatment monitoring and supportive care.

A 7-year-old under-immunized boy presents with 3 days of sore throat, low-grade fever, and progressive odynophagia. Examination reveals a gray, adherent pseudomembrane over both tonsils and soft palate with palatal petechiae and neck adenopathy. There is no stridor and oxygen saturation is 98% on room air. You strongly suspect respiratory diphtheria and have already obtained cultures and started intravenous penicillin G.

Which ONE of the following is the MOST important additional therapy that should be initiated as soon as possible?

Admit to the intensive care unit for observation with serial ECGs but no further specific therapy

Schedule rigid laryngoscopy to aggressively debride the pseudomembrane and improve airway patency

Start nebulized racemic epinephrine and high-dose intravenous dexamethasone

Administer equine diphtheria antitoxin intravenously after assessing for hypersensitivity to equine serum

Perform emergent tonsillectomy to remove the nidus of infection

Tutor-style explanation

Correct answer: D.

Explanation:
Why this option is correct:
Equine diphtheria antitoxin neutralizes circulating diphtheria toxin and is the only therapy that can prevent progression of systemic toxicity once respiratory diphtheria is established. It should be administered as soon as clinical diphtheria is suspected, without waiting for culture confirmation, because toxin-mediated myocarditis and neuropathy may already be evolving. Antibiotics such as penicillin or erythromycin eradicate Corynebacterium diphtheriae and limit further toxin production but do not neutralize toxin that has already been released. Because the product is equine-derived, a focused allergy history and appropriate hypersensitivity precautions are necessary, but these should not unduly delay antitoxin administration.

Why the other options are wrong:
Nebulized racemic epinephrine and intravenous dexamethasone are useful for viral croup and some inflammatory airway disorders but do not address toxin-mediated disease in diphtheria and cannot prevent the systemic complications of myocarditis and neuropathy. They may provide transient symptomatic benefit at best and are not a substitute for antitoxin.

Routine rigid laryngoscopy with aggressive debridement of the pseudomembrane is potentially dangerous in diphtheria. Manipulation can dislodge membrane fragments and precipitate acute airway obstruction or bleeding. Airway instrumentation should only be performed when clinically indicated for obstruction and with extreme caution, not as first-line therapy in a stable child.

Emergent tonsillectomy does not improve outcomes in diphtheria. The pathology is toxin-mediated, not due to a localized tonsillar abscess or peritonsillar collection, and tonsillectomy carries substantial bleeding and airway risks in this setting. It is not recommended as part of standard diphtheria management.

Observation in the intensive care unit with serial ECGs is appropriate as an adjunct because diphtheria-associated myocarditis may develop, but simply admitting for monitoring without timely administration of antitoxin fails to provide the key intervention that alters the course of disease. Cardiac and neurologic monitoring complement, but do not replace, early antitoxin therapy.

Further Reading:
Centers for Disease Control and Prevention. Diphtheria: Pink Book chapter (CDC)
Thomet JM, et al. Access to diphtheria antitoxin for therapy and diagnostics. Clin Infect Dis. 2014 (PubMed)
Diphtheria antitoxin monograph for professionals (Drugs.com)

Additional Concepts:
• Myocarditis is one of the most feared complications of diphtheria and may present with conduction block, arrhythmias, or heart failure days after the onset of pharyngeal disease. Serial ECGs and cardiac enzymes, along with a low threshold for intensive care monitoring, are recommended in moderate to severe cases.
• Neurologic complications of diphtheria include palatal and bulbar palsies, cranial neuropathies, and a delayed demyelinating polyneuropathy resembling Guillain–Barré syndrome. These occur due to toxin-mediated nerve injury and may become apparent after the acute respiratory illness has improved.
• Airway management in diphtheria requires careful planning because blind or traumatic intubation can dislodge pseudomembranes and cause sudden obstruction. If airway compromise is likely, controlled intubation or tracheostomy should be performed by experienced personnel, often with consideration of early surgical airway in severe laryngeal involvement.
• Close contacts of a patient with respiratory diphtheria require prompt evaluation, throat cultures, and antibiotic prophylaxis, along with review and updating of diphtheria vaccination. Immunized individuals can still act as asymptomatic carriers, so chemoprophylaxis and booster immunization may both be indicated.

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The ABOHNS Written Examination (often called the Written Qualifying Examination, or WQE) is a computer-based, proctored, closed-book assessment that covers the full breadth of otolaryngology–head and neck surgery.

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ABOHNS Written Boards (WQE) FAQs

Quick answers to common questions about OtoPrep’s ABOHNS (ABOto) Written Boards / Written Qualifying Examination (WQE) prep.

What’s included in an ABOHNS (WQE) subscription?

All plans include full access to the 8000+ question bank, board-style single-best-answer practice, detailed explanations (including why distractors are wrong), subspecialty analytics, and timed practice for exam-day pacing.

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Yes. Explanations are written to help you learn the concept and avoid common traps, including why distractors don’t fit the stem.

How should I pace ABOHNS Written Boards (WQE) questions?

Use timed blocks to train a steady rhythm, practise skipping when you’re stuck, and return later with a clean head. Mock papers help you pressure-test pacing and stamina so the real exam feels familiar.

Which plan should I choose for the ABOHNS Written Boards (WQE)?

If you want the calmest runway with time to repeat weak areas, choose the 6-month plan. If your exam is closer, the 1–3 month plans suit focused revision blocks and intensive pacing work.

Can I upgrade my plan later?

Yes — if you decide you want a longer runway, you can upgrade by purchasing a longer access plan.

Can I use OtoPrep on mobile or tablet?

Yes. The platform is mobile-friendly with large tap targets and smooth navigation—ideal for short sessions on busy call weeks.

How should I use OtoPrep week-to-week?

Keep it simple: do a set, review the reasoning, flag weak questions, then revisit them on a spaced schedule. Add timed blocks and mock papers as you get closer to exam day.

I’ve subscribed but content isn’t unlocked — what should I do?

First, make sure you’re logged into the same account you used at checkout. If it still isn’t unlocked, contact us via the website contact form with your account email and a screenshot so we can fix it quickly.

Is OtoPrep affiliated with the ABOHNS?

No. OtoPrep is an independent educational platform and is not affiliated with, endorsed by, or sponsored by any examining body. Exam names are used for descriptive purposes only.

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ABOHNS Written Boards (WQE) Question Bank + Timed Mock Exams

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