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DNB Exam — Complete Answer Set

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Question 1: Radiotherapy [10 marks]

a) How does radiotherapy act? [3]

• High-energy photons or particles directly break chemical bonds in DNA, causing single-strand breaks (SSBs) and double-strand breaks (DSBs)
• DSBs are the most lethal — they cannot be accurately repaired and lead to cell death

• Radiation interacts with intracellular water → radiolysis → generates free radicals (hydroxyl radical •OH)
• Free radicals attack DNA, causing strand breaks
• This is the primary pathway of radiation-induced DNA damage
• Oxygen enhances this effect (Oxygen Enhancement Ratio, OER ~2.5–3)

1. Mitotic (reproductive) death — cells die during subsequent divisions
2. Apoptosis — especially in lymphocytes and salivary cells
3. Interphase death — at very high doses

• Most sensitive: G2 and M phases
• Most resistant: late S phase

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b) Dose delivery modifications to increase effectiveness and decrease toxicity [4]

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c) Clinical features of radiation toxicity [3]

• Skin: Erythema → moist desquamation → ulceration (radiation dermatitis)
• Mucosa: Mucositis — painful ulceration, dysphagia, odynophagia
• Salivary glands: Xerostomia, thick ropy saliva
• Larynx: Edema, hoarseness
• Systemic: Fatigue, nausea

• Soft tissue edema
• Radiation-induced hypothyroidism (after neck RT)

• Fibrosis: Trismus (pterygoid fibrosis), neck fibrosis
• Osteoradionecrosis: Mandible — avascular necrosis after dental extraction
• Xerostomia: Permanent if parotids not spared
• Sensorineural hearing loss (cochlear damage)
• Radiation-induced malignancy (latency 10–20 years)
• Cataracts (lens is radiosensitive)
• Spinal cord: Lhermitte's sign (transient) → transverse myelitis (rare, late, permanent)
• Hypothyroidism: 20–30% after neck irradiation
• Carotid stenosis/blowout (rare)

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Question 2: Gene Mapping and Gene Therapy [10 marks]

a) What is gene mapping? [1]

• Genetic (linkage) mapping: Based on recombination frequency during meiosis
• Physical mapping: Determines actual physical location in base pairs on the chromosome

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b) Strategies employed for gene mapping [3]

1. Linkage Analysis:
   • Based on the principle that genes located close together on a chromosome are inherited together (linked)
   • Uses LOD (logarithm of odds) score; LOD ≥3 = significant linkage
   • Useful for Mendelian disorders (e.g., mapping BRCA1)
2. RFLP (Restriction Fragment Length Polymorphism):
   • Uses restriction enzymes to cut DNA at variable sites
   • Differences in fragment lengths used as markers
3. Microsatellite/STR Mapping:
   • Short tandem repeats scattered throughout genome
   • Highly polymorphic — used in disease gene localization
4. GWAS (Genome-Wide Association Studies):
   • Scans entire genome for SNPs (single nucleotide polymorphisms)
   • Used for complex polygenic diseases
5. Physical Mapping Techniques:
   • FISH (Fluorescence In Situ Hybridization) — localizes genes to chromosome bands
   • STS (Sequence-Tagged Sites) — unique landmarks every 100kb
   • YAC (Yeast Artificial Chromosome) libraries
6. Chromosomal deletion mapping:
   • Correlates clinical features with chromosomal deletions (e.g., Wilms tumor → del 11p13)

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c) Viral vectors used for gene therapy [2]

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d) Approaches used in gene therapy [4]

1. Gene Replacement (Gene Augmentation):
   • A functional copy of the defective gene is delivered
   • Used for loss-of-function mutations (e.g., cystic fibrosis CFTR, ADA-SCID)
2. Gene Silencing / RNA Interference:
   • siRNA or antisense oligonucleotides silence overexpressed or mutant genes
   • Used in cancer (oncogene suppression) and viral infections
3. Gene Editing (CRISPR-Cas9):
   • Precise cutting and correction of mutations at specific genomic sites
   • Guide RNA directs Cas9 endonuclease to the target
   • Applications: sickle cell anemia, beta-thalassemia, Duchenne MD
4. Suicide Gene Therapy:
   • HSV-thymidine kinase gene delivered to tumor cells
   • Ganciclovir administered → phosphorylated by TK → toxic to tumor cells
   • "Bystander effect" kills adjacent tumor cells
5. Immunomodulatory Gene Therapy:
   • Genes encoding cytokines (IL-2, IFN-γ, TNF-α) delivered to stimulate anti-tumor immunity
   • CAR-T cell therapy (ex vivo gene modification of T cells)
6. Antisense Therapy:
   • Complementary RNA/DNA strand binds mRNA → prevents translation
   • Fomivirsen (CMV retinitis) — first approved antisense drug

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Question 3: Gamma Knife Radiosurgery [10 marks]

a) Basic principles of gamma knife stereotactic radiosurgery [4]

1. Multiple converging beams:
   • 192 (Perfexion model) cobalt-60 sources arranged in a hemisphere
   • Each beam individually is subtherapeutic, but at the isocenter, beams converge to deliver an ablative dose
   • Surrounding normal brain receives only low doses from each individual beam
2. Stereotactic localization:
   • A stereotactic frame is fixed to the skull under local anesthesia (or frameless system using mask)
   • Coordinates are established in 3D space (x, y, z axes)
   • MRI/CT/angiography maps the target precisely
3. Dose planning (inverse planning):
   • Computer-based dose planning ensures sharp dose falloff at target margins
   • High central dose, steep gradient externally → "conformality"
   • Prescription dose chosen based on target volume and proximity to critical structures
4. Radiobiological basis:
   • Single high-dose fraction causes direct DNA DSBs, vascular endothelial damage, and tumor cell death
   • Dose falloff is so steep that normal tissue 1–2mm away receives very low dose
   • Not suitable for large tumors (>3cm) due to risk of edema
5. Types of sources: Cobalt-60 (Gamma Knife); linear accelerator (LINAC-based SRS); CyberKnife (robotic arm)

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b) Steps involved in treating a patient with gamma knife [4]

1. Pre-treatment workup:
   • High-resolution MRI (Gd-enhanced), CT, MR angiography
   • Neurological evaluation, informed consent
2. Frame application:
   • Leksell stereotactic frame fixed to skull with 4 pins under local anesthesia
   • Frame provides rigid, reproducible 3D coordinate system
3. Imaging for target localization:
   • MRI with frame in place
   • Fiducial markers on frame visible on imaging → establish coordinates
   • Target volume and critical structures (optic nerves, brainstem) delineated
4. Dose planning:
   • Neurosurgeon + radiation oncologist + medical physicist collaborate
   • Leksell GammaPlan software used
   • Isodose curves, conformality index, gradient index optimized
5. Treatment delivery:
   • Patient positioned on treatment couch, helmet (collimator) selected
   • Multiple isocenters ("shots") may be used for irregular targets
   • Session typically 20–90 minutes; painless
6. Post-treatment:
   • Short observation period (4–6 hours)
   • Dexamethasone if edema expected
   • Outpatient discharge; follow-up MRI at 3, 6, 12 months

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c) Limitations of gamma knife [2]

1. Intracranial only — not applicable for extracranial or spinal targets (unlike CyberKnife/SBRT)
2. Size limitation — lesions >3–3.5 cm have higher risk of radiation necrosis and edema; not ideal
3. Single fraction — only one session; if tumor not controlled, re-treatment is limited
4. Frame-based discomfort — invasive frame causes patient discomfort (newer frameless masks available)
5. Delayed response — tumor response may take months; not suitable for emergency decompression
6. Cost — equipment-intensive; not universally available
7. Cannot treat diffuse or multifocal disease — only focal lesions (≤3–4 targets)
8. Risk of radiation necrosis — particularly in previously irradiated fields

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Question 4: Midline Neck Swelling [10 marks]

a) Differential diagnosis of a midline neck swelling [4]

1. Thyroglossal cyst (most common midline neck swelling)
2. Submental lymph node (reactive/malignant)
3. Dermoid cyst (congenital, above hyoid)
4. Plunging ranula (if dissects below mylohyoid)

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b) Clinical presentation of thyroglossal cyst [2]

• Age: Commonest congenital neck mass; usually presents in children (2nd decade peak)
• Site: Midline or slightly to the left of midline, anywhere along the course of the thyroglossal tract (from foramen cecum to pyramidal lobe of thyroid)
  • 65% at/below hyoid; 20% at hyoid; 15% above hyoid
• Nature: Smooth, soft, cystic, non-tender, non-pulsatile swelling
• Pathognomonic sign: Moves upward on protrusion of tongue (due to attachment to foramen cecum via fibrous tract)
• Size: Usually 1–4 cm
• Complications:
  • Infection → abscess formation → fistula (thyroglossal fistula)
  • Malignant transformation (1%): papillary carcinoma most common
• Investigation: USS (cystic midline) + thyroid scan to confirm normal thyroid before surgery

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c) Differences between ectopic and aberrant thyroid [4]

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Question 5: Neck Secondaries, Lymph Node Levels & Dissections [10 marks]

a) Sites for putative biopsies in unknown primary with neck secondaries [2]

1. Nasopharynx — most common hidden primary; Waldeyer's ring
2. Base of tongue (posterior 1/3) — often occult
3. Tonsil/tonsillar fossa — tonsillectomy as diagnostic biopsy
4. Pyriform sinus/hypopharynx — direct laryngoscopy required
5. Supraglottis/subglottis — endoscopic biopsy
6. Postnasal space — PNS endoscopy + biopsies
7. Floor of mouth, oral tongue — inspect and biopsy
8. Thyroid gland — if Level VI/VII nodes involved

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b) Levels of lymph nodes in neck [4]

• Oral cavity/lip → Level I, II
• Oropharynx → Level II, III
• Hypopharynx/larynx → Level II, III, IV
• Thyroid → Level VI, then II–V
• Nasopharynx → Level V, II (Rouvière's node)

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c) Types of neck lymph node dissections [4]

• Removal of Levels I–V + SCM + IJV + Spinal accessory nerve (SAN)
• Morbidity: shoulder drop (SAN), neck contour deformity
• Currently rarely performed

• Levels I–V + preservation of one or more of: SCM, IJV, SAN
• Type I MRND: SAN preserved
• Type II MRND: SAN + IJV preserved
• Type III MRND (Functional ND): SAN + IJV + SCM all preserved
• Most commonly performed for N+ disease

• Only specific levels removed based on primary tumor site
• Supraomohyoid ND: Levels I–III (oral cavity primaries)
• Anterolateral ND: Levels II–IV (oropharynx, larynx, hypopharynx)
• Lateral ND: Levels II–IV
• Central compartment ND: Level VI (thyroid, subglottic)

• Includes additional structures beyond RND (carotid artery, hypoglossal nerve, skin, parotid)
• For advanced/fixed disease

• Injection of radiocolloid/blue dye near tumor
• Identification and excision of first draining node
• Used to assess N0 neck in oral cavity (floor of mouth, tongue)

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Question 6: Chemotherapy Classification & Strategies in Head & Neck [10 marks]

a) Classify chemotherapeutic agents according to their mechanism of action [6]

• Mechanism: Form covalent bonds with DNA → cross-links → strand breaks → inhibit replication
• Subclasses:
  • Nitrogen mustards: Cyclophosphamide, Ifosfamide, Mechlorethamine
  • Nitrosoureas: Carmustine (BCNU), Lomustine (CCNU) — lipid soluble, cross BBB
  • Platinum compounds: Cisplatin, Carboplatin, Oxaliplatin (form intrastrand cross-links in DNA)
  • Alkyl sulfonates: Busulfan
  • Triazines: Temozolomide, Dacarbazine

• Mechanism: Structural analogs of normal metabolites → inhibit DNA/RNA synthesis
  • Antifolates: Methotrexate (inhibits DHFR → depletes THF → blocks purine/thymidylate synthesis)
  • Pyrimidine analogs: 5-Fluorouracil (inhibits thymidylate synthase; false base incorporation); Gemcitabine; Cytarabine
  • Purine analogs: 6-Mercaptopurine, 6-Thioguanine, Fludarabine, Cladribine

• Vinca alkaloids (M-phase specific): Vincristine, Vinblastine, Vinorelbine
  • Mechanism: Bind tubulin → inhibit microtubule polymerization → arrest in metaphase
• Taxanes (M-phase specific): Paclitaxel, Docetaxel
  • Mechanism: Stabilize polymerized microtubules → prevent depolymerization → mitotic arrest
• Podophyllotoxins (G2/S): Etoposide, Teniposide — inhibit Topoisomerase II

• Type II inhibitors: Etoposide, Doxorubicin (intercalation + Topo II inhibition)
• Type I inhibitors: Irinotecan, Topotecan (camptothecins) — inhibit Topo I → DNA strand breaks

• Anthracyclines: Doxorubicin, Epirubicin, Daunorubicin — intercalate DNA + Topo II inhibition + free radicals
• Bleomycin: Causes DNA strand breaks via free radical generation; causes pulmonary fibrosis
• Mitomycin C: Acts as alkylating agent after activation
• Actinomycin D: Intercalates DNA; inhibits RNA polymerase

• Monoclonal antibodies:
  • Cetuximab (anti-EGFR) — used in H&N cancers
  • Bevacizumab (anti-VEGF)
  • Pembrolizumab/Nivolumab (anti-PD-1) — immune checkpoint inhibitors
• Tyrosine kinase inhibitors: Erlotinib, Gefitinib (EGFR-TKI)
• mTOR inhibitors: Everolimus, Temsirolimus
• PARP inhibitors: Olaparib (BRCA-mutated cancers)

• Anti-estrogens: Tamoxifen, Letrozole
• Anti-androgens: Enzalutamide, Bicalutamide

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b) Various chemotherapy strategies in head and neck malignancies [4]

• Most important strategy — standard of care for locally advanced HNSCC
• Chemotherapy (weekly Cisplatin 40mg/m² or 3-weekly Cisplatin 100mg/m²) given during radiotherapy
• Acts as radiosensitizer — enhances RT effect on locoregional disease
• MACH-NC meta-analysis: 8% absolute survival benefit with concurrent CRT

• Given before definitive treatment (surgery or CRT)
• TPF regimen (Docetaxel + Cisplatin + 5-FU) — standard induction regimen (TAX 323, TAX 324 trials)
• Goals: tumor downstaging, organ preservation, treat micrometastases
• Used in: unresectable disease, larynx/hypopharynx preservation

• Given after surgery to eliminate micrometastatic disease
• Used post-operatively in high-risk features (positive margins, extranodal extension)
• Usually concurrent CRT post-operatively (Bernier/Cooper trials — Cisplatin + RT)

• RTOG 91-11 trial: Concurrent CRT superior to induction CT + RT for larynx preservation
• Avoids total laryngectomy in Stage III/IV laryngeal cancer

• For recurrent/metastatic disease
• EXTREME regimen: Cetuximab + Cisplatin + 5-FU (first line; EXTREME trial)
• Pembrolizumab ± Cisplatin/5-FU: CheckMate/KEYNOTE-048 — now 1st-line for PD-L1 expressing tumors
• Monotherapy: Methotrexate, Cetuximab (2nd line)

• Anti-EGFR antibody + RT (Bonner trial) — alternative to CisRT in cisplatin-ineligible patients

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Question 7: PET/PET-CT in Head and Neck [10 marks]

a) Principles of PET (Positron Emission Tomography) [3]

1. ¹⁸F-FDG (fluorine-18 labeled glucose analog) is injected intravenously
2. FDG is taken up by metabolically active cells (tumors, brain, heart) via GLUT transporters
3. Inside the cell, FDG is phosphorylated by hexokinase → FDG-6-phosphate (cannot be further metabolized — metabolic trapping)
4. ¹⁸F undergoes beta-positive decay → emits a positron (β⁺)
5. The positron travels a short distance, then encounters an electron → annihilation reaction
6. Annihilation produces two 511 keV gamma photons emitted at exactly 180° to each other
7. PET scanner detects these coincident photons using ring detectors → determines line of response
8. Tomographic reconstruction (iterative algorithms) generates 3D metabolic maps

• ¹⁸F-FDG: glucose metabolism (most widely used)
• ¹¹C-Methionine: amino acid metabolism (brain tumors)
• ¹⁸F-NaF: bone metabolism (bone mets)
• ¹⁸F-PSMA: prostate cancer

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b) SUV (Standardized Uptake Value) in relation to PET [2]

SUV = Tissue activity (kBq/mL) ÷ [Injected dose (kBq) / Body weight (g)]

• Normal tissue SUV: <2.5
• Malignant lesion: Typically SUV >2.5; higher SUV → more aggressive
• SUVmax: Maximum SUV in the most active voxel of the lesion; most commonly used
• Prognostic value: Higher SUVmax correlates with poorer prognosis in H&N cancers
• Limitations: SUV affected by blood glucose level (diabetics need glucose correction), body composition, time after injection, scanner variability
• Response assessment: Reduction in SUV after treatment indicates response; SUV <3 after chemoradiation suggests complete response

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c) Oncological indications of PET-CT in head and neck [5]

1. Detection of unknown primary — PET-CT detects occult primary in ~25% of patients with cervical lymph node metastasis of unknown primary (targets base of tongue, tonsil, nasopharynx)
2. Staging of head and neck cancers:
   • Regional node assessment (N staging) — superior to CT/MRI for small metabolically active nodes
   • Distant metastasis detection (M staging) — lungs, liver, bones
   • Second primary tumor detection (synchronous) — important in H&N cancers (5–10% synchronous)
3. Post-treatment assessment:
   • Evaluate response after chemoradiation (performed at 8–12 weeks after completion)
   • High negative predictive value (>95%) for residual disease in neck — can avoid planned neck dissection if PET negative
   • PET-NECK trial: PET-CT surveillance non-inferior to planned neck dissection in N2/N3 disease
4. Detection of recurrence:
   • Distinguishes recurrent tumor from post-treatment fibrosis/changes (CT/MRI cannot)
   • Any rising tumor marker or clinical suspicion prompts PET-CT
5. Radiation treatment planning:
   • Biological target volume (BTV) — identifies metabolically active tumor core for dose escalation (dose painting)
   • Better target delineation than CT alone
6. Thyroid cancer: ¹⁸F-FDG PET for Tg-positive, RAI-negative differentiated thyroid cancer; also for medullary/anaplastic thyroid cancer staging
7. Lymphoma staging — Ann Arbor staging, post-treatment Deauville scoring

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Question 8: Lignocaine [10 marks]

a) Mechanism of action of lignocaine [2]

1. Lignocaine exists in equilibrium between ionized (charged) and non-ionized (uncharged) forms
2. The non-ionized form penetrates the lipid bilayer of the nerve membrane
3. Once inside, it ionizes and blocks voltage-gated sodium channels from the inner (cytoplasmic) side
4. Binding is use-dependent/frequency-dependent — blocks channels more in rapidly firing nerves
5. Blocks Na⁺ channel → prevents depolarization → no action potential → no nerve conduction
6. Smaller unmyelinated fibers (C-fibers — pain, autonomic) blocked first; large myelinated fibers (motor) last

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b) Maximum safe dose of lignocaine infiltration [2]

• Adrenaline causes vasoconstriction → reduces systemic absorption → allows higher dose
• Standard 2% lignocaine contains 20 mg/mL
• At 7 mg/kg in a 70 kg adult: 490 mg ≈ 25 mL of 2% lignocaine with adrenaline
• Avoid adrenaline in: end arteries (digits, nose tip, penis), ischemic vascular disease, uncontrolled hypertension

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c) Adverse drug reactions of lignocaine [3]

1. Circumoral/tongue numbness (early sign)
2. Tinnitus, dizziness, visual disturbances
3. Slurred speech, confusion, drowsiness
4. Muscle twitching → Convulsions (tonic-clonic)
5. CNS depression → Respiratory arrest (high doses)

• Bradycardia, hypotension
• PR prolongation, QRS widening
• Heart block, ventricular fibrillation (rare)

• True allergy rare (amide group; more common with ester anesthetics)
• Reactions usually due to preservatives (methylparaben) or adrenaline
• Urticaria, angioedema, anaphylaxis (rare)

• Chondrotoxicity (intra-articular injections)
• Myotoxicity at high concentrations

• High doses or metabolite (o-toluidine) → oxidizes hemoglobin → metHb → cyanosis

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d) Plester's technique of local anesthesia for ear surgeries [3]

1. Superior (12 o'clock position): Injection at the spine of Henle (suprameatal spine); just posterior to the EAC opening superiorly
2. Posterior (6 o'clock position): Injection posterior and inferior to the EAC
3. Anterior-superior: Anterior to the canal at the superior aspect
4. Anterior-inferior: Anterior to the canal at the inferior aspect

• Skin of the bony and cartilaginous external auditory canal
• Tympanic membrane
• Adjacent mastoid cortex and auricle

• Bloodless field (adrenaline vasoconstriction)
• Allows manipulation of the tympanic membrane, canal skin, and cortical mastoid under local anesthesia
• Can be supplemented with auriculotemporal nerve block (for anterior EAC)

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Question 9: Dysplasia of the Larynx [10 marks]

a) Cytological features of dysplasia [3]

1. Nuclear changes (most important):
   • Nuclear enlargement (high N:C ratio)
   • Hyperchromasia (increased DNA staining)
   • Irregular nuclear membrane (pleomorphism)
   • Prominent/multiple nucleoli
   • Abnormal mitotic figures (in severe dysplasia)
2. Cellular changes:
   • Loss of normal cellular polarity
   • Individual cell keratinization (dyskeratosis)
   • Cellular pleomorphism
   • Increased mitotic activity, including abnormal mitoses
   • Loss of intercellular bridges
3. Architectural changes (on histology):
   • Loss of normal stratification
   • Disordered maturation from basal to surface layer

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b) Grades of dysplasia [3]

• Simple hyperplasia → Abnormal (basal/parabasal cell) hyperplasia → Atypical hyperplasia → CIS

• Mild dysplasia: ~5% progression to carcinoma
• Moderate dysplasia: ~20–25%
• Severe dysplasia: ~30–40%
• CIS: ~50–60% progress to invasive carcinoma

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c) Management of carcinoma in situ of the glottis [4]

• Hoarseness (persistent, progressive)
• Leukoplakia or erythoplakia on cord
• Microlaryngoscopy essential for diagnosis + biopsy

• Cold steel (microflap technique) or laser (CO₂ laser)
• CO₂ laser cordectomy (Type I or II — WHO classification of laser cordectomies)
• Allows histological examination of specimen
• Recurrence rate ~20–25%; repeat endoscopic treatment for recurrence

• Useful when CIS is extensive/bilateral or recurrent
• External beam RT, total dose 60–66 Gy
• Excellent local control (~90–95%) with voice preservation
• Preferred by some centers for bilateral/extensive CIS
• Risk: chronic radiation laryngitis, later difficulty detecting recurrence (mucosal changes)

• Photosensitizer (Photofrin) + laser activation → singlet oxygen → tumor cell death
• Option for recurrent/multifocal disease
• Limited availability

• After treatment, close endoscopic surveillance every 3 months for 2 years, then 6-monthly
• Any recurrence/progression → repeat biopsy

• With treatment, CIS has excellent prognosis
• ~15–25% eventually develop invasive carcinoma if untreated

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Question 10: Floor of Mouth Reconstruction & Nasolabial Flap [10 marks]

a) Reconstruction options following floor of mouth resection surgeries [6]

• For small defects (<2 cm)
• Direct mucosal closure
• Risk: Tongue tethering, restricted mouth opening

• Small-to-medium superficial defects after laser excision
• STSG laid over defect; immobilized with bolster
• Suitable when no bone exposed

• Nasolabial flap (see part b)
• Buccal mucosal advancement flap — for small anterior floor defects
• Tongue flap — for small posterior defects; reliable blood supply

• PMMC (Pectoralis Major Myocutaneous Flap):
  • Workhorse of H&N reconstruction
  • Pedicle: thoracoacromial artery
  • Good bulk; used for large defects with segmental mandibulectomy
  • Disadvantages: bulky, hair-bearing (in males), poor sensory recovery
• Deltopectoral (DP) flap:
  • Fasciocutaneous; perforators from internal mammary artery
  • Used for anterolateral defects; limited arc of rotation

• Titanium plates ± fibula for mandible reconstruction
• Dental implants placed in neomandible post-reconstruction

• Maintain tongue mobility (avoid tethering)
• Preserve mandibular continuity when possible
• Restore sensory function (sensate RFFF — medial antebrachial cutaneous nerve coaptation)
• Watertight closure to prevent salivary fistula

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b) Blood supply and uses of the nasolabial flap [4]

• Superiorly based flap: Supplied by facial artery and its branches:
  • Superior labial artery
  • Angular artery
  • Infraorbital perforators
• Inferiorly based flap: Supplied by perforators from the facial artery (submental and buccal branches)
• The flap is random pattern (subdermal plexus) in the nasolabial fold — rich vascular territory

• Skin of nasolabial fold is thin, well-vascularized, and color-matches facial skin
• Can be islanded on its pedicle or used as advancement/rotation flap
• Can be tubed for intraoral use

1. Floor of mouth reconstruction — small-to-medium defects post-resection
2. Buccal mucosal defects — after resection of buccal carcinoma
3. Palatal reconstruction — small palatal fistulas
4. Alveolar defects — gingival/alveolar mucosal coverage
5. Tongue reconstruction — partial glossectomy defects (small)

• Local tissue — excellent color and texture match
• Robust blood supply — reliable
• Donor site closed primarily → scar hidden in nasolabial fold
• Single-stage or two-stage (for pedicle division at 3 weeks)

• Limited reach and bulk
• Hair-bearing (in males) when used intraorally
• Two-stage procedure for intraoral use (pedicle division required)
• Not suitable for large defects

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Summary — All 10 DNB Questions Answered

• Q3 (Gamma knife) and Q7 (PET-CT) are frequently asked in DNB Head & Neck — memorize the PET-NECK trial and SUV formula
• Q5 — know the Robbins classification levels cold with boundaries and primary drainage
• Q8 — Plester's technique is very specific to ENT/H&N — 4 quadrant injections at the EAC
• Q10 — for flap questions, always tabulate (flap type → pedicle → indication) for maximum marks