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Hi, I'm a medical student in, uh, GMC, the Neil Grease in OT Medical College, final year MBBS, okay? So I need you to guide me to this pathway. I'm already six months, it's over, okay? It's July month, July 11 or 12, I think so. So let's start our process, okay? So what we need to do is that I'm going to tomor-- uh, start nose in ENT. What you need to do is that give me question and answers detailly, okay? 20 marks in nose. Each and every topic covers. And then fill in the blanks also I need from ENT, okay? Fill in the blanks like 20 to 35, okay? And two marks, three marks, four marks, because that was going to be a pattern. And every-- each and every topic is needed, okay?

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I now have substantial content from the ENT textbooks. I have enough information to compile a thorough Q&A set. Let me now write the complete answer.Here is your complete ENT (Nose) Q&A study material, covering all topics across all mark formats. This is exam-ready for both university theory and NEET PG.

🩺 ENT - NOSE: Complete Q&A Study Material

Final Year MBBS | University Theory + NEET PG

SECTION A: 2-MARK QUESTIONS (Short Notes / One-liners)

TOPIC 1: ANATOMY OF NOSE & PARANASAL SINUSES

Q1. What is the blood supply of the nasal septum? A: The nasal septum is supplied by:
  • Sphenopalatine artery (branch of internal maxillary artery) - posterior septum
  • Anterior ethmoidal artery (from ophthalmic artery) - superior septum
  • Greater palatine artery - floor
  • Superior labial artery (from facial artery) - anteroinferior
  • Little's area (Kiesselbach's plexus) = anastomosis of all five vessels at anteroinferior septum - the commonest site of epistaxis.
Q2. What is Kiesselbach's plexus / Little's area? A: It is a vascular plexus on the anteroinferior part of the nasal septum where five arteries anastomose:
  1. Anterior ethmoidal artery
  2. Sphenopalatine artery
  3. Greater palatine artery
  4. Superior labial artery
  5. Septal branch of superior labial
It is the most common site of anterior epistaxis (90% of all epistaxis).
Q3. Name the paranasal sinuses and their drainage. A:
SinusDrains into
MaxillaryMiddle meatus (via hiatus semilunaris)
Anterior ethmoidMiddle meatus
FrontalMiddle meatus (via frontonasal duct)
Posterior ethmoidSuperior meatus
SphenoidSphenoethmoidal recess
Nasolacrimal ductInferior meatus
Mnemonic: Middle meatus = FMAE (Frontal, Maxillary, Anterior Ethmoid). Superior meatus = Posterior Ethmoid. Sphenoethmoidal recess = Sphenoid.
Q4. What is the nasal cycle? A: The nasal cycle is the alternating congestion and decongestion of the two nasal cavities occurring every 2-4 hours. It is controlled by the autonomic nervous system. The total nasal resistance remains constant. In patients with DNS, the nasal cycle becomes clinically significant as obstruction alternates between sides.
Q5. What is the internal nasal valve? A: The internal nasal valve is the narrowest part of the nasal airway (10-15 degrees angle) formed between the caudal edge of the upper lateral cartilage and the nasal septum. Any compromise here causes significant nasal obstruction. The Cottle maneuver tests its patency.
Q6. What is the ostiomeatal complex (OMC)? A: The OMC is a functional unit in the middle meatus comprising:
  • Uncinate process
  • Middle turbinate
  • Infundibulum
  • Hiatus semilunaris
  • Bulla ethmoidalis
It is the final common pathway for drainage of the frontal, maxillary, and anterior ethmoid sinuses. Obstruction here leads to chronic rhinosinusitis.

TOPIC 2: RHINITIS

Q7. Define allergic rhinitis. What mediates its symptoms? A: Allergic rhinitis (AR) is an IgE-mediated inflammatory condition of the nasal mucosa triggered by exposure to allergens (dust mites, pollen, animal dander). Symptoms are mediated by histamine, leukotrienes, prostaglandins, and tryptase released from mast cell degranulation. Symptoms include sneezing, watery rhinorrhea, nasal congestion, and itching.
Q8. What is vasomotor rhinitis? A: Also called idiopathic rhinitis or non-allergic rhinitis. It is characterized by nasal congestion and rhinorrhea without identifiable allergic cause. Triggers include cold air, humidity changes, strong smells, smoke, emotional stress, and exercise. It results from an imbalance of autonomic (parasympathetic overactivity) control of the nasal mucosa. Skin tests and IgE levels are negative.
Q9. What is atrophic rhinitis? Name the causative organism. A: Atrophic rhinitis (ozaena) is a chronic nasal condition with progressive atrophy of the nasal mucosa, turbinates, and underlying bone. Features:
  • Foul-smelling nasal discharge (ozaena)
  • Large, empty nasal cavity
  • Crusting
  • Paradoxical nasal obstruction (patient feels blocked despite wide nasal cavity)
Causative organism: Klebsiella ozaenae (primary). Others: Staphylococcus, Proteus mirabilis, E. coli.
Q10. What is rhinitis medicamentosa? A: Rhinitis medicamentosa is rebound nasal congestion caused by prolonged use (>5 days) of topical nasal decongestants (oxymetazoline, xylometazoline). It leads to a cycle of dependency. Treatment is by gradual withdrawal of the decongestant and substitution with intranasal corticosteroids.

TOPIC 3: SINUSITIS

Q11. What are the symptoms of acute maxillary sinusitis? A:
  • Facial pain/pressure over the cheek, worse on bending forward
  • Nasal congestion and mucopurulent discharge
  • Fever, malaise
  • Toothache (upper teeth)
  • Post-nasal drip
  • Nasal endoscopy: mucopus in middle meatus
Q12. Define chronic rhinosinusitis (CRS). A: CRS is defined as inflammation of the nose and paranasal sinuses for >12 weeks with at least 2 of the following symptoms:
  • Nasal congestion/obstruction
  • Nasal discharge (anterior/posterior)
  • Facial pain/pressure
  • Reduction/loss of smell
With objective evidence on endoscopy or CT scan. It may occur with nasal polyps (CRSwNP) or without nasal polyps (CRSsNP).
Q13. What is the Caldwell-Luc operation? When is it done? A: Caldwell-Luc is a surgical procedure for chronic maxillary sinusitis. An antrostomy is made through the anterior wall of the maxillary sinus via a sublabial incision (canine fossa). A counter-opening (antrostomy) is then made in the inferior meatus for drainage. It has been largely replaced by Functional Endoscopic Sinus Surgery (FESS). It is still used for tumors and in cases where FESS is not feasible.
Q14. What is a mucocele of the paranasal sinus? A: A mucocele is an epithelial-lined, mucus-containing cyst that completely fills a paranasal sinus. It is expansile and causes bony erosion. Most common in frontal and ethmoid sinuses. It can cause orbital displacement (proptosis, diplopia) or intracranial complications. Treatment is endoscopic marsupialization (drainage), not complete removal.

TOPIC 4: NASAL POLYPS

Q15. What is the difference between antrochoanal polyp and ethmoidal polyp? A:
FeatureAntrochoanal PolypEthmoidal Polyp
OriginMaxillary antrumEthmoid sinuses
SideUnilateralUsually bilateral
NumberSingleMultiple
AgeChildren/young adultsAdults
AllergyNot usuallyOften associated
ConsistencySoft, myxoidFirm, gelatinous
RecurrenceRare if completely removedCommon
Q16. What conditions are associated with nasal polyps? A:
  • Chronic rhinosinusitis (most common)
  • Allergic rhinitis
  • Asthma (Samter's triad)
  • Aspirin sensitivity
  • Cystic fibrosis (commonest nasal polyp in children)
  • Kartagener's syndrome (bronchiectasis + situs inversus + sinusitis)
  • Churg-Strauss syndrome

TOPIC 5: EPISTAXIS

Q17. Classify epistaxis. A:
  • By site:
    • Anterior (90%) - from Little's area/Kiesselbach's plexus
    • Posterior (10-20%) - from sphenopalatine artery branches; more serious
  • By cause:
    • Local: trauma, DNS, rhinitis, polyps, tumors, foreign body
    • Systemic: hypertension (most common systemic cause), coagulopathy, blood disorders (leukemia, hemophilia), liver disease, Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia)
Q18. What is Osler-Weber-Rendu disease? A: Also called Hereditary Hemorrhagic Telangiectasia (HHT). It is an autosomal dominant condition characterized by telangiectasias in the skin, mucous membranes (especially nasal and GI), and visceral AVMs (lungs, brain, liver). Recurrent epistaxis is the hallmark. Diagnosis by clinical criteria (Curacao criteria). Treatment: laser coagulation, embolization.

TOPIC 6: DNS (Deviated Nasal Septum)

Q19. What causes DNS? A:
  • Trauma (birth injury, accidental trauma) - most common acquired cause
  • Developmental - unequal growth of septum and its bony framework
  • Congenital - pressure during intrauterine life or passage through birth canal (forceps)
  • Minor trauma in childhood causes microfractures that heal with cartilage bending
Q20. What is "paradoxical nasal obstruction" in DNS? A: In a patient with DNS, the patient may feel more congested on the opposite (wider) side rather than the deviated side. This is because the widened side accommodates a compensatorily hypertrophied turbinate that causes obstruction. The actual smaller (deviated) side paradoxically feels more open. This is called paradoxical nasal obstruction.

SECTION B: 3-MARK QUESTIONS

Q1. Describe the pathophysiology of allergic rhinitis. A:
  1. Sensitization phase: Allergen exposure β†’ antigen processing by APCs (macrophages, dendritic cells) β†’ presentation to TH2 lymphocytes β†’ IL-4, IL-13 secretion β†’ B cell class switching β†’ IgE production β†’ IgE binds to mast cells and basophils in nasal mucosa
  2. Early phase reaction (minutes after re-exposure): Allergen cross-links IgE on mast cells β†’ degranulation β†’ release of histamine, prostaglandins, leukotrienes, tryptase β†’ sneezing, rhinorrhea, itching within minutes
  3. Late phase reaction (4-8 hours later): Cytokine-mediated recruitment of eosinophils, basophils, T cells β†’ chronic mucosal inflammation β†’ nasal congestion predominates
  4. This leads to nasal hyperreactivity to both specific allergens and non-specific stimuli.
Q2. Classify non-allergic rhinitis (NAR). A: (From Cummings Otolaryngology)
Types of NAR:
  1. Idiopathic/Vasomotor rhinitis - triggered by environmental changes (cold air, temperature, humidity), strong smells, smoke, emotions, exercise
  2. Non-Allergic Rhinitis with Eosinophilic Syndrome (NARES) - eosinophilia on nasal smear, no allergy
  3. Hormonal rhinitis - pregnancy (20% of pregnant women, worse in 3rd trimester), hypothyroidism, acromegaly - caused by estrogen-induced glandular activity, increased mucopolysaccharide production
  4. Medication-induced rhinitis - ACE inhibitors, beta-blockers, aspirin, oral contraceptives, rhinitis medicamentosa
  5. Atrophic rhinitis - primary (Klebsiella ozaenae) or secondary (post-surgical, radiation, granulomatous)
  6. Gustatory rhinitis - spicy foods, alcohol β†’ parasympathetic reflex
  7. Occupational rhinitis - chemical/dust exposure at workplace
Q3. What is the management of posterior epistaxis? A:
  1. First aid: Pinch the soft part of the nose, lean forward, apply ice pack over nose
  2. Assessment: Check vitals, IV access, blood cross-match for severe bleed
  3. Anterior nasal pack: First try BIPP pack or Merocel pack in anterior cavity
  4. Posterior nasal pack: If anterior packing fails - Foley catheter balloon or Brighton balloon placed in nasopharynx to tamponade posterior bleeding
  5. Cauterization: Chemical (silver nitrate) or electrical cautery under endoscopy
  6. Endoscopic sphenopalatine artery ligation: Surgical option if packing fails
  7. Embolization: Angiographic superselective embolization of internal maxillary artery branches. Success rate 91-97% with complication rate 0-3%
  8. Treat cause: Correct coagulopathy, control hypertension
Q4. Write short notes on FESS (Functional Endoscopic Sinus Surgery). A:
  • Principle: Restore normal mucociliary clearance by opening the Ostiomeatal Complex (OMC) - the functional drainage unit of sinuses - with minimal tissue removal
  • Indications: Chronic rhinosinusitis not responding to medical therapy, nasal polyps (CRSwNP), recurrent acute rhinosinusitis (>4 episodes/year), mucoceles, antrochoanal polyps, CSF rhinorrhea
  • Procedure: Endoscopic removal of uncinate process β†’ opening ethmoid bullae β†’ wide middle meatal antrostomy β†’ frontal and sphenoid sinusotomy as needed
  • Advantages over Caldwell-Luc: No external incision, less morbidity, tissue-preserving, better visualization, day surgery
  • Complications: Orbital injury (diplopia, blindness), CSF leak, bleeding, anosmia
Q5. Describe the features of atrophic rhinitis. A:
  • Synonym: Ozaena (primary atrophic rhinitis)
  • Causes: Primary - Klebsiella ozaenae infection; Secondary - previous radical turbinectomy, radiation, granulomatous disease (TB, sarcoid, syphilis)
  • Pathology: Atrophy of nasal mucosa, ciliated columnar β†’ squamous metaplasia, atrophy of submucosal glands and vessels, resorption of turbinate bone
  • Symptoms:
    • Nasal crusting with foul-smelling discharge (ozaena) - patient often unaware
    • Paradoxical nasal obstruction (large nasal cavity but feels blocked)
    • Anosmia / hyposmia
    • Headache, epistaxis
  • Signs: Spacious nasal cavity filled with greenish-brown crusts
  • Treatment: Medical - nasal irrigation with saline, estrogen drops, glucose-glycerine drops; Surgical - Young's operation (closure of nostril), submucosal injection of Teflon

SECTION C: 4-MARK QUESTIONS

Q1. Classify nasal polyps. Describe the clinical features and management of nasal polyps. A:
Classification:
  1. Ethmoidal polyps - bilateral, multiple, associated with allergy/CRS/asthma, from ethmoid sinuses
  2. Antrochoanal polyp (Killian's polyp) - single, unilateral, arises from maxillary antrum, grows posteriorly through the posterior fontanelle to the choana. Seen in children and young adults
  3. Specific polyps - malignant (antrochoanalimicking), meningocele, encephalocele (pulsatile, should never be biopsied blindly)
Clinical Features of Ethmoidal Polyps:
  • Progressive bilateral nasal obstruction
  • Hyposmia or anosmia
  • Watery or mucopurulent rhinorrhea
  • Mouth breathing, snoring
  • May cause broadening of the nasal bridge (frog face deformity in severe cases)
  • On examination: pale/grey, insensitive, smooth grape-like masses in nasal cavity
Management:
  • Medical: Intranasal corticosteroids (first-line) - budesonide, fluticasone; Oral steroids for rapid reduction; Antihistamines for allergic component; Treat underlying CRS/allergy
  • Surgical (FESS): For polyps not responding to medical therapy; microdebrider-assisted polypectomy + ethmoidectomy; wide antrostomy
  • Recurrence: Common in ethmoidal polyps; long-term intranasal steroids post-op to prevent recurrence
Antrochoanal Polyp Management:
  • FESS with removal of both nasal and antral components through posterior fontanelle; supplementary inferior meatal approach if needed; Low recurrence if completely removed
Q2. Discuss the diagnosis and management of deviated nasal septum (DNS). A:
Definition: Deviation of the nasal septum from the midline causing symptoms, most commonly nasal airway obstruction.
Causes:
  • Birth trauma (forceps delivery, tight birth canal)
  • Post-natal trauma
  • Unequal growth / developmental
  • Congenital intrauterine pressure
Clinical Features:
  • Unilateral nasal obstruction (alternating in some cases due to nasal cycle)
  • Paradoxical obstruction (see Q20 above)
  • Recurrent sinusitis (especially maxillary)
  • Epistaxis (from deviated side due to turbulent airflow drying the mucosa)
  • Headache
  • Anosmia
  • Secondary turbinate hypertrophy on the contralateral (concave) side
Examination:
  • Anterior rhinoscopy: deviated cartilaginous or bony septum
  • Cottle maneuver: improvement of nasal airflow on lateral traction of cheek (tests internal nasal valve)
  • Nasal endoscopy / CT PNS: for surgical planning
Management:
  1. Conservative: Nasal decongestants, saline irrigation, treat associated rhinitis
  2. Surgical - Septoplasty:
    • Indicated when medical treatment fails and symptoms are significant
    • Procedure: Hemitransfixion/Kilians incision β†’ elevate mucoperichondrial flap β†’ resect or reposition deviated portion β†’ maintain L-strut (1 cm dorsal + 1 cm caudal strip) to preserve tip and dorsal support
    • Postoperative: No packing generally; suture quilting of flaps with 5-0 plain suture; thin Silastic sheets only in perforations
  3. SMR (Submucous Resection) - older technique; more radical; risk of saddle nose deformity
  4. Septorhinoplasty - if external deformity also present
Complications of septoplasty:
  • Septal perforation (if bilateral mucosal tears without interposition graft)
  • Saddle nose deformity (over-resection)
  • Loss of tip support
  • Anosmia, CSF leak (rare)
Q3. Discuss epistaxis - causes, classification, and management. A:
Definition: Bleeding from the nose - can be anterior (90%) or posterior (10-20%).
Causes - Local:
  • Trauma (nose-picking - most common in children, nasal fractures)
  • Deviated nasal septum (septal spur - dries mucosa)
  • Rhinitis, sinusitis
  • Foreign body (unilateral foul-smelling discharge in child)
  • Nasal polyps, angiofibroma (profuse bleed in adolescent male)
  • Tumors (carcinoma of nasal cavity/sinus)
Causes - Systemic:
  • Hypertension (most common systemic cause in adults, causes posterior epistaxis)
  • Coagulopathies - hemophilia, von Willebrand disease, ITP
  • Drugs - aspirin, warfarin, heparin, NSAIDs
  • Blood dyscrasias - leukemia, aplastic anemia
  • Liver disease (reduced clotting factors)
  • Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu) - autosomal dominant; telangiectasias + recurrent epistaxis
  • Vitamin C and K deficiency
  • Renal failure
Management of Anterior Epistaxis:
  1. Sit upright, lean forward
  2. Pinch soft part of nose for 10-15 minutes (continuous)
  3. Apply ice pack over nose/forehead
  4. If continues: silver nitrate chemical cauterization of Little's area
  5. Anterior nasal packing: Merocel, BIPP (Bismuth Iodoform Paraffin Paste) for 24-48 hours
Management of Posterior Epistaxis:
  1. Posterior nasal packing: Brighton balloon / Foley catheter balloon (10 mL) placed via nose into nasopharynx
  2. Endoscopic cauterization of sphenopalatine artery
  3. Surgical ligation: sphenopalatine artery, anterior ethmoidal artery, internal maxillary artery
  4. Angiographic embolization: superselective catheterization of internal maxillary and facial arteries; 91-97% success rate; useful in elderly and posterior bleeds not responding to packing
  5. Treat underlying cause: antihypertensives, correct coagulopathy

SECTION D: 20-MARK LONG ANSWER QUESTIONS

Q1. Classify rhinitis. Discuss the etiopathogenesis, clinical features, investigations, and treatment of allergic rhinitis. (20 marks)

CLASSIFICATION OF RHINITIS:
A. Allergic Rhinitis (AR):
  1. Seasonal (hay fever) - pollens
  2. Perennial - dust mites, animal dander, mold
  3. ARIA Classification: Intermittent vs Persistent; Mild vs Moderate-Severe
B. Non-Allergic Rhinitis:
  1. Idiopathic/Vasomotor rhinitis
  2. NARES (Non-Allergic Rhinitis with Eosinophilic Syndrome)
  3. Infectious rhinitis - viral (common cold), bacterial
  4. Atrophic rhinitis (Ozaena)
  5. Hormonal rhinitis - pregnancy, hypothyroidism, acromegaly
  6. Medication-induced - ACE inhibitors, rhinitis medicamentosa
  7. Gustatory rhinitis
  8. Granulomatous rhinitis - TB, sarcoidosis, Wegener's (GPA), leprosy, syphilis
ETIOPATHOGENESIS OF ALLERGIC RHINITIS:
Genetic Factors: Atopic individuals (personal/family history of atopy); imbalance of TH1 vs TH2 immunity - TH2 predominance promotes IgE production.
Sensitization Phase:
  • Allergen deposited on nasal mucosa β†’ epithelial cells secrete TSLP (thymic stromal lymphopoietin) β†’ maturation of TH2-promoting dendritic cells
  • Antigen processed by APCs (macrophages, dendritic cells, Langerhans cells) β†’ presented to TH2 lymphocytes
  • TH2 cells secrete IL-4, IL-5, IL-13 β†’ B cells undergo IgE class switching β†’ allergen-specific IgE produced
  • IgE binds to high-affinity FcΞ΅RI receptors on mast cells and basophils in nasal mucosa
Early Phase Reaction (Immediate, within minutes of re-exposure):
  • Allergen cross-links IgE on mast cells β†’ mast cell degranulation
  • Preformed mediators released: Histamine (sneezing, rhinorrhea, itching), tryptase, heparin
  • Newly synthesized mediators: Prostaglandin D2, leukotriene C4/D4/E4 (congestion), bradykinin
  • Result: Sneezing, itching, watery rhinorrhea, early congestion
Late Phase Reaction (4-8 hours later):
  • Cytokine (IL-4, IL-5, eotaxin) mediated recruitment of eosinophils, basophils, T cells, neutrophils
  • Chronic mucosal eosinophilic inflammation
  • Nasal hyperreactivity to non-specific stimuli
  • Nasal congestion predominates
CLINICAL FEATURES:
  • 4 cardinal symptoms: Sneezing (paroxysmal), watery rhinorrhea, nasal congestion, nasal/ocular/palatal pruritus
  • Ocular: Allergic conjunctivitis (red, watery, itchy eyes) in 50%
  • Signs: Pale/bluish, boggy nasal mucosa; clear watery discharge; allergic shiners (dark circles under eyes); allergic salute (transverse nasal crease from repeated rubbing); adenoid facies in chronic childhood AR
  • Nasal smear: Eosinophilia (>25% eosinophils)
INVESTIGATIONS:
  1. Nasal smear (cytology): Eosinophilia confirms allergy
  2. Skin prick test (SPT): Gold standard for identifying specific allergens; wheal >3mm = positive
  3. Serum total IgE: Elevated in atopics
  4. Specific IgE (RAST/ImmunoCAP): Identifies allergen-specific IgE; useful when SPT is not possible
  5. Nasal provocation test: Direct allergen challenge - research setting
  6. Nasal endoscopy: Pale, edematous mucosa, clear secretions; rule out polyps
  7. CT PNS: If sinusitis is suspected
TREATMENT:
Step 1 - Allergen Avoidance:
  • Dust mite control (mattress covers, washing bedding in hot water)
  • HEPA filters, avoid pets, pollen avoidance (stay indoors during peak pollen times)
Step 2 - Pharmacotherapy (ARIA stepwise):
Drug ClassExamplesActionUse
Intranasal corticosteroidsFluticasone, Budesonide, MometasoneReduce mucosal inflammationFirst-line for persistent AR
Oral antihistamines (2nd gen)Cetirizine, Loratadine, FexofenadineBlock H1 receptorsSneezing, rhinorrhea, itching
Intranasal antihistaminesAzelastine, OlopatadineLocal H1 blockadeRapid onset; unilateral symptoms
Oral decongestantsPseudoephedrineΞ±-adrenergic; vasoconstrictionShort-term congestion
Leukotriene antagonistsMontelukastBlock LT receptorsEspecially with asthma
Intranasal cromoglicateSodium cromoglicateMast cell stabilizerProphylactic; safe in pregnancy
Anti-IgEOmalizumabBlocks free IgESevere, refractory cases
BiologicsDupilumab (IL-4/13 blocker)Reduces TH2 inflammationCRSwNP, severe AR
Step 3 - Allergen Immunotherapy (AIT):
  • Subcutaneous immunotherapy (SCIT) or Sublingual immunotherapy (SLIT)
  • Gradual desensitization - works by inducing T-regulatory cells, shifting TH2 β†’ TH1
  • Only disease-modifying treatment
  • Indicated: Moderate-severe AR not controlled by pharmacotherapy; monosensitized patients
  • Duration: 3-5 years

Q2. Epistaxis - Causes, Classification, Clinical features, Management (20 marks)

(See 4-mark Q3 above for detailed content. For a full 20-mark answer, expand each section as follows:)
Full Structure:
  1. Definition + Anatomy of nasal blood supply (Little's area, Woodruff's plexus)
  2. Classification (anterior/posterior; local/systemic)
  3. Local causes (detailed)
  4. Systemic causes (detailed) - Hypertension, coagulation disorders, HHT, drugs
  5. Clinical features - Anterior vs Posterior; assessment of severity
  6. Investigations: CBC, PT/aPTT, BT/CT, BP measurement, nasal endoscopy, angiography if embolization planned
  7. Management:
    • First aid
    • Anterior packing (methods, materials)
    • Posterior packing (Foley catheter technique)
    • Cauterization
    • Surgical ligation (sphenopalatine artery, anterior ethmoidal artery)
    • Angiographic embolization (success 91-97%)
  8. Management of HHT epistaxis specifically
  9. Complications of nasal packing

Q3. Discuss DNS (Deviated Nasal Septum) - Etiology, Pathology, Clinical Features, Investigations, Management (20 marks)

(Combine all content from 4-mark Q2 above and expand with:)
  1. Detailed anatomy of nasal septum (cartilaginous, bony components)
  2. Types of septal deviation (anterior, posterior, vertical, horizontal, C-shaped, S-shaped, spur)
  3. Histopathology of deviated septum and turbinate changes
  4. Full investigation protocol (anterior rhinoscopy, nasal endoscopy, CT PNS)
  5. Detailed septoplasty steps (Kilians incision, mucoperiosteal flap elevation, L-strut preservation)
  6. Complications of surgery
  7. Role of turbinate surgery in addition to septoplasty

SECTION E: FILL IN THE BLANKS (35 Questions)

  1. The most common site of anterior epistaxis is ______. (Little's area / Kiesselbach's plexus)
  2. The blood vessel most commonly responsible for posterior epistaxis is the ______. (Sphenopalatine artery)
  3. The causative organism of primary atrophic rhinitis is ______. (Klebsiella ozaenae)
  4. The narrowest part of the nasal airway is the ______. (Internal nasal valve)
  5. The foul smell in atrophic rhinitis is called ______. (Ozaena)
  6. The classical sign of Hereditary Hemorrhagic Telangiectasia in the nose is recurrent ______. (Epistaxis)
  7. The maxillary sinus drains into the ______ meatus. (Middle)
  8. The sphenoid sinus drains into the ______. (Sphenoethmoidal recess)
  9. The nasolacrimal duct drains into the ______ meatus. (Inferior)
  10. Rhinitis medicamentosa is caused by prolonged use of topical ______. (Nasal decongestants / oxymetazoline)
  11. The most common benign tumor of the nose in adolescent males that causes profuse bleeding is ______. (Juvenile Nasopharyngeal Angiofibroma / JNA)
  12. The 'frog face deformity' is seen in massive ______. (Nasal polyposis)
  13. Nasal polyps in children are most commonly associated with ______. (Cystic fibrosis)
  14. An antrochoanal polyp arises from the ______ sinus. (Maxillary)
  15. The alternating nasal congestion between the two nostrils occurring every 2-4 hours is called the ______. (Nasal cycle)
  16. Samter's triad consists of nasal polyps, asthma, and ______ sensitivity. (Aspirin)
  17. The functional endoscopic sinus surgery (FESS) targets the ______ as the key drainage pathway. (Ostiomeatal complex / OMC)
  18. The gold standard test for identifying allergens in allergic rhinitis is the ______. (Skin prick test)
  19. The only disease-modifying treatment for allergic rhinitis is ______. (Allergen immunotherapy / AIT)
  20. The L-strut preserved during septoplasty consists of ______ cm dorsal and ______ cm caudal strip. (1 cm / 1 cm)
  21. The procedure of closing the nasal opening to treat atrophic rhinitis is called ______. (Young's operation)
  22. The operation for chronic maxillary sinusitis via canine fossa incision is called ______. (Caldwell-Luc operation)
  23. Mucoceles most commonly occur in the ______ and ______ sinuses. (Frontal / Ethmoid)
  24. Granulomatous rhinitis due to Wegener's granulomatosis is now called ______. (Granulomatosis with polyangiitis / GPA)
  25. The IgE class switching in allergic rhinitis is mediated by cytokines ______ and ______. (IL-4 / IL-13)
  26. Eosinophilia >25% on nasal smear is diagnostic of ______. (Allergic rhinitis / NARES)
  27. NARES stands for ______. (Non-Allergic Rhinitis with Eosinophilic Syndrome)
  28. The posterior nasal pack for epistaxis uses a ______ balloon. (Foley catheter / Brighton balloon)
  29. Pregnancy-induced rhinitis affects approximately ______% of pregnant women. (20%)
  30. The success rate of angiographic embolization for intractable epistaxis is ______. (91-97%)
  31. The inverted papilloma of the nose is also called ______ papilloma. (Schneiderian)
  32. The biologic drug that blocks free IgE used in severe allergic rhinitis is ______. (Omalizumab)
  33. Kartagener's syndrome is a triad of sinusitis, bronchiectasis, and ______. (Situs inversus)
  34. The type of rhinitis caused by spicy food is called ______. (Gustatory rhinitis)
  35. The histological change in atrophic rhinitis is conversion of ciliated columnar epithelium to ______. (Squamous epithelium / stratified squamous metaplasia)
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