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- •Contents
- •1.1.9 Laryngeal Atresia
- •1.1.10 Laryngeal Webs
- •1.1.11 Congenital Subglottic Stenosis
- •1.1.12 Laryngeal Cleft
- •1.1.13 Tracheoesophageal Fistula
- •1.1.14 Tracheal Bronchus
- •1.2.2 Mesenchyme Development
- •1.2.4 Lung Development
- •1.2.4.1 Embryonic Stage
- •1.2.4.2 Pseudoglandular Stage
- •1.1.1 Oral Cavity
- •1.1.2 Nasal Cavity
- •1.1.3 Palate
- •1.1.4 Primitive Pharynx
- •1.1.5 Upper Airway Anomalies
- •1.1.6 Cleft Lip/Palate
- •1.1.7 Choanal Atresia
- •1.1.8 Laryngomalacia
- •1.2.4.3 Canalicular Stage
- •1.2.4.4 Saccular Stage
- •1.2.4.5 Alveolar Stage
- •1.2.5 Congenital Respiratory System Defects
- •1.2.5.1 Tracheal Agenesis
- •1.2.5.2 Congenital Tracheal Stenosis
- •1.2.5.3 Lung Agenesis
- •1.2.5.4 Lung Hypoplasia
- •References
- •2.1 Introduction
- •2.2 Nasal Cavity
- •2.2.1 Vestibule
- •2.2.2 Respiratory Mucosa
- •2.2.3 Olfactory Mucosa
- •Supporting Cells
- •Basal Cell
- •Olfactory Receptor Cell (Bipolar Neuron)
- •Brush Cell (Microvillar Cell)
- •2.2.3.2 The Lamina Propria
- •2.2.3.3 Olfactory Glands (Bowman’s Glands)
- •2.3 Paranasal Sinuses
- •2.4 Pharynx
- •2.5 Larynx
- •2.6 Trachea
- •2.6.1.1 Ciliated Columnar Cells
- •2.6.1.2 Goblet Cells
- •2.6.1.3 Brush Cells
- •2.6.1.4 Basal Cells
- •2.6.1.5 Enteroendocrine System Cells (Kulchitsky Cells or DNES Cells)
- •2.6.2 Lamina Propria
- •2.7 Lungs
- •2.7.1 Pleura
- •2.7.2 Bronchi
- •2.7.3 Bronchioles
- •2.7.3.1 Terminal Bronchioles
- •2.7.3.2 Respiratory Bronchioles
- •2.7.4 Ductus Alveolaris
- •2.7.5 Alveoli
- •2.7.5.2 Type II Alveolar Cell (Septal Cell, Large Alveolar Cell)
- •References
- •3.1.1.3 Nerves
- •Ophthalmic Division
- •Maxillary Division
- •Parasympathetic Nerve Supply
- •3.1.1.4 Bony Anatomy
- •3.1.1.5 Cartilaginous Pyramid
- •3.1.1.6 Structure
- •External Nasal Anatomy
- •Internal Nasal Anatomy
- •3.1.2 Nasal Physiology
- •3.1.2.1 Nasal Airflow
- •3.1.2.2 Abnormal Nasal Physiology
- •3.2.1 Larynx Anatomy
- •Cricoid Cartilage
- •Thyroid Cartilage
- •Epiglottis
- •Arytenoid Cartilages
- •Corniculate Cartilages
- •Cuneiform Cartilages
- •Extrinsic Ligaments
- •Intrinsic Ligaments
- •Laryngeal Cavity
- •Piriform Recesses
- •Cricothyroid Muscles
- •Posterior Cricoarytenoid Muscles
- •Lateral Cricoarytenoid Muscles
- •Transverse Arytenoid Muscle
- •Thyroarytenoid Muscles
- •Superior Laryngeal Nerve
- •Arteries
- •Veins
- •Lymphatics
- •Swallowing
- •Respiration
- •Phonation
- •3.2.2.1 Reflex Glottic Closure
- •References
- •4.1 Introduction
- •4.2.1 Choanal Atresia
- •4.2.2 Pyriform Aperture Stenosis
- •4.2.3 Cleft Lip Nasal Deformity
- •4.2.4 Nasolacrimal Duct Cysts
- •4.2.5 Encephaloceles
- •4.3 Craniofacial Anomalies
- •4.3.1 Pierre Robin Syndrome
- •4.3.2 Treacher-Collins Syndrome
- •4.3.3 Crouzon Syndrome
- •4.3.4 Down Syndrome
- •4.3.5 Apert Syndrome
- •4.4.1 Thyroglossal Duct Cyst
- •4.4.2 Laryngomalacia
- •4.4.3 Vocal Fold Paralysis
- •4.4.5 Subglottic Stenosis
- •4.4.6 Subglottic Hemangioma
- •4.4.7 Laryngeal Cysts
- •4.4.8 Laryngeal Cleft
- •4.5 Conclusion
- •References
- •5.1 Innate Immunity
- •5.2 Adaptive Immunity
- •References
- •6.1 Introduction
- •6.2 Innate Immunity
- •6.3 Adaptive Immunity
- •References
- •7.1 Introduction
- •References
- •8: Respiratory Microbiome
- •8.1 Introduction
- •8.2.1 Childhood Asthma
- •8.2.2 Asthma Exacerbation
- •8.3 Bacteriome
- •8.4 Virome
- •8.5 Mycobiome
- •References
- •9.1 Introduction
- •References
- •10.1 Introduction
- •10.3.3 The Appointment Process, Explained
- •10.3.5 Parental Involvement
- •10.4 Coordinating Care When Your Child Is Ill
- •10.4.3 Exhibit Cohesion
- •10.6 Conclusion
- •References
- •11.1 Introduction
- •11.2 Nasal Cavity
- •11.2.1 Choanal Atresia
- •11.2.2 Rhinosinusitis
- •11.2.4 Juvenile Nasopharyngeal Angiofibroma
- •11.3 Pharynx
- •11.4 Nasopharynx
- •11.4.1 Adenoid Hypertrophy
- •11.4.2 Nasopharyngeal Carcinoma
- •11.5 Oropharynx
- •11.5.1 Thyroglossal Duct Cyst
- •11.6 Hypopharynx
- •11.6.1 Retropharyngeal Abscess
- •11.6.2 Lymphatic Malformation
- •11.6.4 Lymphoma
- •11.6.5 Rhabdomyosarcoma
- •11.7 Larynx
- •11.7.1 Subglottic Stenosis
- •11.7.2 Laryngotracheal Papillomatozis
- •11.7.3 Croup
- •11.7.4 Epiglottitis
- •11.7.5 Foreign Body Aspiration
- •References
- •12.2.1 Plain Radiography
- •12.2.1.1 The Thymus
- •Tracheal Buckling
- •Hilum
- •Diaphragm
- •Mediastinal Borders
- •Lung Opacities
- •Cystic Lung Diseases
- •Pulmonary İnterstitial Emphysema (PIE)
- •Unilateral Hyperlucent Lung
- •12.2.2 Fluoroscopy
- •12.2.3 Ultrasound
- •12.2.4 Computed Tomography
- •12.2.5 Magnetic Resonance Imaging (MRI)
- •12.2.6 Angiography
- •12.2.7 Positron Emission Tomography (PET)
- •12.3 Conclusion
- •References
- •13.1 Introduction
- •13.2 Nasal Diagnostic Procedures
- •13.2.1 Indications
- •13.2.2 Contraindications
- •13.2.3 Anatomical Features
- •13.2.4 Technical Considerations
- •13.2.5 Technique
- •13.2.5.1 First Pass
- •13.2.5.2 Second Pass
- •13.2.5.3 Third Pass
- •13.3 Flexible Laryngoscopy
- •13.4 Direct Laryngoscopy
- •13.5 Video Laryngoscopy
- •13.5.1 Indications
- •13.5.2 Contraindications
- •13.5.3 Outcomes
- •13.5.4 Equipment
- •13.5.5 Approach Considerations
- •References
- •14.1 Upper Airways
- •14.2.3 Laryngeal Pathologıes
- •References
- •15.1 Introduction
- •15.2 Airway Measurements
- •References
- •16.1 Introduction
- •16.2 Background
- •References
- •17: Allergen Testing: Purpose, Procedure, Interpretation
- •17.1 Introduction
- •17.2 Tests
- •17.2.1 Skin Tests
- •17.2.3 Component Resolved Diagnosis (CRD)
- •17.2.4 Tryptase
- •17.2.5 Basophil Activation Test (BAT)
- •17.2.6 Provocation Tests
- •17.2.7 Nasal sIgE
- •17.2.8 Nasal Smear Eosinophilia
- •17.2.9 Eosinophilic Cationic Protein (ECP)
- •References
- •18: Smell Testing: Purpose, Procedure, Interpretation
- •18.1 Introduction
- •18.2 Possible Olfactory Disorder Diagnosis
- •18.2.1 Conductive Defects
- •18.2.3 Inherited Disorders
- •18.2.3.1 Hormonal Disturbances
- •18.4 Odor Threshold Tests
- •18.8.1 Butanol Threshold Test
- •18.8.1.1 The Penn State University Odor Identification Exam
- •18.8.2 Cross-Cultural Smell Identification Test
- •18.8.3 Sniffin’ Sticks
- •References
- •19: Taste Testing: Purpose, Procedure, Interpretation
- •19.1 Introduction
- •19.2 Definitions
- •19.2.1 Taste Dysfunction Abnormalities
- •19.4.1 Taste Dysfunction
- •19.4.2 COVID-19
- •19.5 Taste Disorder Diagnosis
- •19.6.2 Magnitude Matching
- •19.6.3 Spatial Test
- •References
- •20.1 Introduction
- •20.2 Primary Otalgia Causes
- •20.2.1 Auricle
- •20.2.1.1 Infections
- •20.2.1.2 Trauma
- •20.2.1.3 Allergic Angioedema
- •20.2.1.4 Thermal Damage
- •20.2.2 External Auditory Canal
- •20.2.2.1 Otitis Externa
- •20.2.2.2 Malignant Otitis Externa
- •20.2.2.3 Eczematous Dermatitis
- •20.2.2.4 Furunculosis
- •20.2.2.5 Foreign Body
- •20.2.2.6 Cerumen Impaction
- •20.2.2.7 Tumors
- •20.2.3 Middle Ear
- •20.2.3.1 Acute Otitis Media
- •20.2.3.3 Eustachian Tube Dysfunction
- •20.2.3.4 Cholesteatoma
- •20.2.3.5 Trauma
- •20.3 Secondary Otalgia Causes
- •20.3.1 Oropharyngeal Infections
- •20.3.2 Dental Causes
- •20.3.3 Auricular Lymphadenitis
- •20.3.4 Neck Abscess
- •20.3.5 Parotitis
- •20.3.6 Temporomandibular Joint Dysfunction
- •20.3.7 Sinusitis
- •20.4 Differential Diagnosis
- •References
- •21.1 Introduction
- •21.2 Bacterial Otitis Externa
- •21.3 Acute Otitis Media
- •21.4 Chronic Suppurative Otitis Media
- •21.5 Foreign Body
- •21.5.1 Cerumen
- •21.5.2 Tympanostomy Tube Drainage
- •21.5.3 Traumatic Cerebrospinal Fluid Otorrhea
- •21.5.5 Necrotizing Otitis Externa (Malignant External Otitis)
- •21.5.6 Neoplasms
- •21.5.7 Polyps
- •21.5.8 Otomycosis
- •21.5.9 First Branchial Cleft Cysts
- •21.5.10 Cholesteatoma
- •21.5.11 Spontaneous Cerebral Spinal Fluid Otorrhea
- •References
- •22.1 Introduction
- •22.4 Congenital Causes
- •22.4.1 Choanal Atresia
- •22.4.2 Pyriform Apertura Stenosis
- •22.4.3 Nasal Midline Congenital Masses
- •22.4.3.1 Nasal Dermoid Cyst
- •22.4.3.2 Nasal Glioma
- •22.4.3.3 Encephalocele (Encephalo-Meningocele)
- •Differential Diagnosis
- •22.4.3.4 Nasolacrimal Duct Cyst (Dacryocystocele)
- •22.5 Infectious Causes
- •22.5.1.1 Rhinitis Etiology
- •22.5.2 Neonatal Rhinitis
- •22.5.3 Bacterial or Viral Rhinitis
- •22.5.4 Iatrogenic Rhinitis
- •22.5.5 Infectious Rhinitis (Rhinosinusitis)
- •22.6 Adenoid Hypertrophy
- •22.7 Inflammatory Causes
- •22.7.1 Allergic Rhinitis
- •22.7.2 Nonallergic Rhinitis
- •22.7.3 Eosinophilic Nonallergic Rhinitis (NARES)
- •22.7.4 Nasal Polyp
- •22.7.5 Antrochoanal Polyp
- •22.7.6 Inferior Turbinate Hypertrophy
- •22.8 Neoplasia
- •22.8.1 Benign Tumors (Juvenile Nasopharyngeal Angiofibroma)
- •22.8.2 Malignant Tumors
- •22.9 Systemic Causes
- •22.9.1 Cystic Fibrosis
- •22.9.2 Primary Ciliary Dyskinesia
- •22.10 Trauma/Iatrogenic Causes
- •22.10.1 Nasal Trauma-Septal Hematoma
- •22.10.2 Septum Deviation
- •22.10.3 Nasal Foreign Bodies
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Allergic Rhinitis
- •23.4 Non-allergic Rhinitis
- •23.5 Infectious Rhinitis
- •23.6.1 Vasomotor Rhinitis
- •23.7 Evaluation
- •23.8 Diagnosis
- •23.9 Treatment
- •23.10 Prognosis
- •23.11 Conclusion
- •References
- •24.1 Introduction
- •24.2 Pathogenesis
- •24.3 Diagnosis
- •24.3.1 History
- •24.3.2 Examination
- •24.4 Differential Diagnoses
- •24.5 CSF Rhinorrhea
- •24.5.1 CSF Physiology
- •24.5.1.1 Pathogenesis
- •24.6 Diagnosis
- •24.6.1 Chemical Diagnosis
- •24.6.2 Imaging Diagnosis
- •24.7 Treatment
- •24.7.1 Surgical Technique
- •References
- •25.1 Introduction
- •25.1.1 Waldeyer Ring
- •25.3 Anatomy
- •25.3.1 Lymphatic Drainage
- •25.3.1.1 Nerve Supply
- •25.6 Tonsillary Hypertrophy
- •25.7 Physical Examination
- •25.8.1 Obstructive Sleep Apnea
- •References
- •26.1 Introduction
- •26.5 Halitosis Physiopathology
- •26.6.1 Oral Halitosis (Intraoral Halitosis, Oral Malodor)
- •26.6.1.1 Periodontal Infections
- •26.6.1.2 Tongue Oriented Halitosis
- •26.6.1.3 Peritonsillar Abscess
- •26.7 Paranasal Sinus Diseases
- •26.8 Adenoid Vegetation
- •26.9 Chronic Pharyngitis
- •26.10 Chronic Tonsillitis
- •26.11 Tonsillolith
- •26.12 Non-Oral Halitosis
- •26.13 Gastroesophageal Reflux
- •26.14 Diagnosis
- •26.14.1 Organoleptic Measurement
- •26.14.2 Sulfur Monitoring
- •26.14.2.1 Indirect Methods
- •26.14.2.3 Ammonia Monitoring
- •26.14.2.4 Polymerase Chain Reaction (PCR)
- •26.15 Physical Examination
- •References
- •27.1 Introduction
- •27.2 Epidemiology
- •27.4 Diagnosis
- •27.5.1 Clinical Assessment
- •27.6 Treatment
- •27.6.1 Voice Therapy
- •27.7 Phonosurgery
- •References
- •28.1 Introduction
- •28.2 Epidemiologic Characteristics
- •28.3 Swallowing Physiologic Phases
- •28.3.1.1 Prematurity
- •28.3.1.2 Neuromuscular
- •28.3.1.5 Cardiopulmonary Disease
- •28.4 Symptoms
- •28.5 Clinical Feeding Assessment
- •28.7 Flexible Endoscopic Swallowing Evaluation
- •28.8 Imaging
- •28.9 Endoscopic Assessments
- •28.9.1 High-Resolution Manometry
- •28.10 Medical Management
- •28.11 Surgical Management
- •28.11.1 Ankyloglossia
- •28.11.2 Laryngomalacia
- •28.11.3 Laryngeal Cleft
- •28.12 Conclusions
- •References
- •29.1 Introduction
- •29.2 Reactive Lymph Node Enlargements
- •29.3 Vaccines
- •29.4 Acute Suppurative Lymphadenitis
- •29.6 Granulomatous Lymphadenitis
- •29.6.1 Mycobacterial Infection
- •29.6.2 BCG Vaccine
- •29.6.3 Cat-Scratch Disease
- •29.6.4 Sarcoidosis
- •29.6.5 Kikuchi-Fujimoto Disease
- •29.7 Malignancies
- •29.8 Diagnosis
- •References
- •30.1 Introduction
- •30.2 Upper Airway Cough Syndrome
- •30.3 Chronic Rhinosinusitis
- •30.5 Otogenic Cough
- •30.6 Laryngeal Clefts
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.5.1 Vocal Cord Disfunction (VCD)
- •31.5.2 Obstructive Sleep Apnea Syndrome (OSAS)
- •31.5.3 Allergic or Non-Allergic Rhinitis
- •31.6 Conclusion
- •References
- •32.1 Introduction
- •32.2.1 Non-massive Hemoptysis
- •32.2.2 Massive Hemoptysis
- •32.4 Diagnostic Evaluation
- •32.4.1 History
- •32.4.1.1 Infection Warning Signs
- •32.4.1.2 Choking
- •32.4.1.3 Exposures
- •32.4.1.4 Underlying Medical Problems
- •32.4.2 Physical Examination
- •32.4.3 Laboratory Evaluation
- •32.4.4 Imaging
- •32.5.1 Respiratory Illness
- •32.5.3 Trauma
- •32.5.4 Hemoptysis Mimics
- •References
- •33.1 Introduction
- •33.6 Conclusion
- •References
- •34: Pediatric Allergic Rhinitis: Otolaryngology Perspective
- •34.1 Introduction
- •34.2 Epidemiology
- •34.2.1 Prevalence
- •34.2.2 Risk factors
- •34.3.1 Classical Pathway
- •34.3.2 Nasal Pathway
- •34.4.2 Physical Examination
- •34.4.3 Diagnostic Tests
- •34.4.4 Nasal Cytology
- •34.4.5 Imaging
- •34.5.1 Adenoid Hypertrophy
- •34.5.2 Nasal Septal Deviation
- •34.5.3 Chronic Rhinosinusitis
- •34.5.4 Turbinate Hypertrophy
- •34.5.5 Nasal Foreign Body
- •34.5.6 Other Clinical Conditions
- •34.6.1 Saline Irrigation (Douching)
- •34.7 Treatment
- •34.7.1 Oral Antihistamines
- •34.7.2 Intranasal Steroids
- •34.7.3 Leukotriene Inhibitors
- •34.7.5 Oral Steroids
- •34.7.6 Intranasal Antihistamines
- •34.7.7 Immunotherapy (Sublingual-Subcutaneous)
- •34.8 Conclusion
- •References
- •35: Allergic Rhinitis: Pediatric Pulmonologist Perspective
- •35.1 Introduction
- •35.2.1 Epidemiological Relationship
- •35.2.4 Immunopathology
- •35.2.7 Non-pharmaceutical Treatment Method
- •35.2.8 Pharmaceutical Medication Policy
- •35.2.9 Immunotherapy Against Allergens
- •35.6 Conclusion
- •References
- •References
- •37.1 Introduction
- •37.2 Adenoid Hypertrophy
- •37.7 Preoperative Evaluation
- •37.8 Contraindications
- •37.9 Complications
- •37.9.1 Bleeding
- •37.9.2 Hypernasality
- •37.9.3 Surgical Traumas
- •37.9.4 Torticollis
- •37.9.5 Otitis Media
- •37.9.6 Psychological Trauma
- •37.9.7 Nasopharyngeal Stenosis
- •37.9.8 Recurrence
- •37.10 Postoperative Care
- •37.11 Surgery
- •37.12.1 Adenoiditis
- •References
- •38.1 Introduction
- •38.2 Anatomy
- •38.2.1 Palatine Tonsils (Faucial Tonsils)
- •38.2.2 Lingual Tonsil
- •38.2.3 Adenoids (Pharyngeal Tonsil)
- •38.2.4 Tubal Tonsils
- •38.5.1 Viral Tonsillitis
- •38.5.2 Bacterial Tonsillitis
- •38.5.3 Candida
- •38.6.1 Suppurative Complications
- •38.6.1.1 Peritonsillar Abscess (Quincy Tonsil)
- •Lemierre’s Syndrome
- •38.6.2 Nonsuppurative Complications
- •38.6.2.1 Acute Rheumatic Fever
- •38.6.2.2 Poststreptococcal Glomerulonephritis
- •38.6.2.3 Scarlet Fever
- •38.6.2.6 Palmoplantar Pustulosis (PPP)
- •38.6.2.7 IgA Nephropathy
- •38.7 Clinical Manifestation
- •38.7.1 Infection
- •38.7.2 Obstruction
- •38.7.3 Neoplasia
- •38.8 Diagnosis
- •38.8.2 Physical Examination
- •38.8.3 Laboratory
- •38.8.4 Imagining
- •38.8.5 Polysomnography
- •38.9 Treatments
- •38.9.1 Medical Treatment
- •38.9.2 Surgery
- •38.9.2.2 Tonsillectomy
- •38.9.3.1 Intraoperative Complications
- •38.9.3.4 Postoperative Long-Term Complications (>weeks)

32
E. T. Uluer et al.
pneumocytes.” These vesicles are multilamellar bodies containing concentric or
parallel lamellae inside, surrounded by a unit membrane with a diameter of 1–2μm
at the ultrastructural level. Histochemical investigations have revealed these structures to be rich in phospholipids, glycosaminoglycans, and proteins. This surfactant
is vital, reducing surface tension, enhancing lung compliance, stabilizing alveoli,
and providing immunity against pathogens, particularly in allergic responses [9].
The surfactant, comprising 90% lipids and 10% protein, coats the inner surfaces of
alveoli as a lm. When the alveolar epithelium is damaged, type II alveolar cells
proliferate and differentiate into the damaged cell [4, 5].
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Structural andPhysiological Basis
oftheUpper Respiratory Tract
OğuzhanOğuz, NurayBayar Muluk, andFeliciaManole
3.1 Nasal Anatomy andPhysiology
3.1.1 Anatomy oftheNose
The external nose consists of paired nasal bones and upper and lower lateral cartilages. Internally, the nasal septum divides the nasal cavity into a right and left side.
The lateral nasal wall consists of inferior and middle turbinates and occasionally a
superior or supreme turbinate bone. The opening of the sinuses also is found under
the middle turbinates on the lateral nasal wall. The lacrimal system drains into the
nasal cavity below the anterior inferior aspect of the inferior turbinates [1].
As in the rest of the upper respiratory tract, nasal membranes are composed of
ciliated pseudostratied glandular columnar epithelium. Cilia beat in unison to propel mucus from the nasal cavity and paranasal sinuses toward the nasopharynx
where it can be swallowed. Mucociliary transport relies on mucus production and
ciliary function. Normally, the nose and paranasal sinuses produce approximately 1
quart of mucus in 24h. The amount of mucus produced can more than double when
the nose and/or sinuses are inamed. Mucus contains IgA, immunoglobulin E, and
muramidase. A study by Uzeloto etal. indicated that mucociliary clearance is negatively impacted by active and passive smoking [2].
3
O. Oğuz
Department of Audiology, Health Services Vocational School, Istanbul Nişantaşı University,
Istanbul, Turkey
Dr. Oğuzhan Oğuz Wellnose Clinic, Istanbul, Turkey
N. Bayar Muluk (*)
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, Turkey
F. Manole
Department of ENT, Faculty of Medicine, University of Oradea, Oradea, Romania
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_3
33

34
O. Oğuz et al.
Blood and autonomic nerve supply control secretions and the level of congestion
of nasal membranes. General innervation to the nose is from the autonomic nervous
system; the parasympathetic nerves supply the resting tone and control secretions.
Contributions of nerve supply are from the facial nerve originating at the inferior
salivatory nucleus and following along the distribution of the facial nerve through
the sphenopalatine ganglion. Blood supply to the nose comes from branches of the
internal and external carotid artery systems. Terminal branches of the internal maxillary artery supply most mucosal surfaces of the nasal cavity. Contributions from
the ophthalmic artery of the internal carotid artery system supply the posterior
aspect of the nasal cavity [1].
Olfactory nerve endings originate in the olfactory bulb under the frontal lobe and
pass directly through the cribriform plate as second-order neurons entering the nasal
cavity. Olfactory nerves are found on the superior portion of the septum, superior
turbinates, and cribriform region [1].
3.1.1.1 Skin andSoft Tissues
Like the underlying bony-cartilaginous framework of the nose, the overlying
skin may also be divided into vertical thirds. The skin of the upper third is fairly
thick but tapers into a thinner, mid-dorsal region. The inferior third regains the
thickness of the upper third owing to the more sebaceous nature of the skin in
the nasal tip. The dorsal skin is usually the thinnest of the three sections of the
nose. The difference in skin thickness must be appreciated during dorsal reduction [3].
The nasal muscles are encountered deep into the skin and consist of four principal groups: the elevators, the depressors, the compressor, and the dilators. The elevators include the procerus and levator labii superioris alaeque nasi. The depressors
are made up of the alar nasalis and depressor septi nasi. The compressor of the nose
is the transverse nasalis, whereas the dilators are the dilator naris anterior and posterior. The muscles are interconnected by an aponeurosis termed the nasal supercial musculoaponeurotic system (SMAS) [4].
The internal nasal lining consists of squamous epithelium in the vestibule. This
transitions to pseudostratied ciliated columnar respiratory epithelium with abundant seromucinous glands within the nose [4].
3.1.1.2 Blood Supply andLymphatics
The nose, like the rest of the face, has an abundant blood supply. The arterial supply
to the nose may be principally divided into (1) branches from the internal carotid,
namely, the branches of the anterior and posterior ethmoid arteries from the ophthalmic artery, and (2) branches from the external carotid, namely, the sphenopalatine, greater palatine, superior labial, and angular arteries [4].
The external nose is supplied by the facial artery, which becomes the angular
artery coursing over the superomedial aspect of the nose. The sellar and dorsal
regions of the nose are supplied by branches of the internal maxillary artery (namely,
the infraorbital) and ophthalmic arteries (which are from the internal carotid system) [4].

3 Structural andPhysiological Basis oftheUpper Respiratory Tract
35
Internally, the lateral nasal wall is supplied by the sphenopalatine artery posteroinferiorly and by the anterior and posterior ethmoid arteries superiorly. The nasal
septum also derives its blood supply from the sphenopalatine and the anterior and
posterior ethmoid arteries with the added contribution of the superior labial artery
(anteriorly) and the greater palatine artery (posteriorly). The Kiesselbach plexus, or
the Little area, represents a region in the anteroinferior third of the nasal septum,
where all three of the chief blood supplies to the internal nose converge [4].
Veins in the nose essentially follow the arterial pattern. They are signicant for
their direct communication with the cavernous sinus and for their lack of valves;
these features potentiate the intracranial spread of infection. Even with the abundant
blood supply of the nose, smoking does compromise postoperative healing [4].
Lymphatics arise from the supercial mucosa and drain posteriorly to the retropharyngeal nodes and anteriorly to the upper deep cervical nodes and/or submandibular glands [4].
3.1.1.3 Nerves
The sensation of the nose is derived from the rst two branches of the trigeminal
nerve. The following outline effectively delineates the respective sensory distribution of the nose and face of the trigeminal nerve [4].
Ophthalmic Division
The ophthalmic division includes the following [4]:
• Lacrimal: Skin of lateral orbital area except lacrimal gland
• Frontal: Skin of forehead and scalp, including the supraorbital (eyelid skin, fore-
head, and scalp) and supratrochlear (medial eyelid and medial forehead) skin
• Nasociliary: Skin of the nose and mucous membrane of anterior nasal cavity.
On a more detailed level, the nasociliary portion of the ophthalmic division
includes the following [4]:
• Anterior ethmoid: Anterior half of nasal cavity: (1) internal: ethmoid and frontal
sinuses and (2) external: nasal skin from rhinion to tip
• Posterior ethmoid: Superior half of the nasal cavity, namely, the sphenoid and
ethmoids
• Intratrochlear: Medial eyelids, palpebral conjunctiva, nasion, and bony dorsum
Maxillary Division
The maxillary division includes the following [3]:
• Maxillary
• Infraorbital: External nares
• Zygomatic
• Superior posterior dental
• Superior anterior dental: Mediates sneeze reex

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O. Oğuz et al.
• Sphenopalatine: Divides into lateral and septal branches and conveys sensation
from posterior and central regions of the nasal cavity
Parasympathetic Nerve Supply
The parasympathetic supply is derived from the greater supercial petrosal
(GSP) branch of cranial nerve VII.The GSP joins the deep petrosal nerve (sympathetic supply), which comes from the carotid plexus to form the vidian nerve
in the vidian canal. The vidian nerve travels through the pterygopalatine ganglion (with only the parasympathetic nerves forming synapses here) to the lacrimal gland and glands of the nose and palate via the maxillary division of the
trigeminal nerve [4].
3.1.1.4 Bony Anatomy
Superiorly, the paired nasal bones are attached to the frontal bone (see the images
below). Superolaterally, they are connected to the lacrimal bones, and inferolaterally, they are attached to the ascending processes of the maxilla. Posterosuperiorly,
the bony nasal septum is composed of the perpendicular plate of the ethmoid, shown
in the second image below. Posteroinferiorly lies the vomer, which in part forms the
choanal opening into the nasopharynx. The oor consists of the premaxilla and the
palatine bones [4].
The lateral nasal walls contain three pairs each of small, thin, shell-like bones:
the superior, middle, and inferior conchae, which form the bony framework of the
turbinates. Lateral to these curved structures lies the medial wall of the maxillary sinus.
Inferior to the turbinates lies a space called a meatus, with names that correspond to the above turbinate, e.g., superior turbinate and superior meatus. The
roof of the nose internally is formed by the cribriform plate of the ethmoid.
Posteroinferior to this structure, sloping down at an angle, is the bony face of the
sphenoid sinus [4].
3.1.1.5 Cartilaginous Pyramid
The cartilaginous septum extends from the nasal bones in the midline above to the
bony septum in the midline posteriorly, then down along the bony oor. It assumes
a quadrangular shape. Its upper half is anked by two triangular-to-trapezoidal cartilages, called the upper lateral cartilages, which are fused to the dorsal septum in
the midline and attached to the bony margin of the pyriform aperture laterally by
loose ligaments. The inferior ends of the upper lateral cartilages are free. The internal area or angle formed by the septum and upper lateral cartilage constitutes the
internal valve. Adjacent sesamoid cartilages may be found lateral to the upper lateral cartilages in the broareolar connective tissue. These are found variably [4].
Beneath the upper lateral cartilages lie the lower lateral cartilages, shown below.
The paired lower lateral cartilages swing out from medial attachments to the caudal
septum in the midline, called the medial crura, to an intermediate crus area. They
nally are out superolaterally as the lateral crura. These cartilages are frequently
mobile, in contradistinction to the upper lateral cartilages [4].

3 Structural andPhysiological Basis oftheUpper Respiratory Tract
37
3.1.1.6 Structure
External Nasal Anatomy
The rst image below depicts the external nasal anatomy. Nasal subunits include the
dorsum, sidewalls, hemilobules, alae, soft triangles, and columella [5]. Ethnic inuences can result in different appearances of the nose [6] as follows: Caucasian,
leptorrhine; African American, platyrrhine; Hispanic, paraleptorrhine; and Asian,
subplatyrrhine. The external valve is a variable area dependent on the size, shape,
and strength of the lower lateral cartilage [4].
Internal Nasal Anatomy
The septum is a midline bony and cartilaginous structure that divides the nose into
two similar halves. Regarding the lateral nasal wall and paranasal sinuses, the superior, middle, and inferior concha form the corresponding superior, middle, and inferior meatus on the lateral nasal wall. The superior meatus is the drainage area for the
posterior ethmoid cells and the sphenoid sinus. The middle meatus provides drainage of the anterior ethmoid and the maxillary and frontal sinuses. The inferior
meatus provides drainage of the nasolacrimal duct [5].
The internal nasal valve involves the area bounded by upper lateral cartilage,
septum, nasal oor, and anterior head of the inferior turbinate. This makes up the
narrowest portion of the nasal airway in the leptorrhine nose. Generally, an angle
wider than 15° is needed in this area. The width of the nasal valve can be increased
with spreader grafts and aring sutures [4].
3.1.2 Nasal Physiology
3.1.2.1 Nasal Airflow
Air ows superiorly into the nares, determined by its position and the anterior
nasal valve. The airstream then turns posteriorly approximately 90° and ows
into the nasopharynx. The airstream then turns inferiorly 90° through the pharynx and larynx and ows into the trachea toward the lungs. The anterior nasal
valve is located 1.5–2cm posterior to the anterior nares and is the narrowest
portion of the upper airway. The narrow portion of the upper airway allows close
contact between the airstream and mucosal surfaces. Humidication occurs by
evaporation of moisture from the mucosal blanket. Air is humidied to 75–80%.
Warming of inspired air to 36°C results from contact between air and the rich
blood supply of the nasal membranes, especially the inferior turbinate
mucosa [1].
Adults condition more than 14,000L of air/day, requiring more than 680 g of
water, approximately 20% of our daily water intake [3].
The sniff is also an important part of nasal airow; it provides a way to force air
into the superior nasal vault and into better contact with the olfactory mucosa.
Information on nasal airow also can be found in the Medscape Reference article
Nasal Aerodynamics [1].

38
With regard to the human nasal cycle, Williams and Eccles proposed a model for
the central control of airow patterns, in which in-phase and reciprocal airow
changes are explained through the incorporation of a hypothalamic center and two
brainstem half centers [7, 8].
O. Oğuz et al.
3.1.2.2 Abnormal Nasal Physiology
Environmental allergies are the most common causes of inammation of nasal
membranes, followed by inhaled irritants (e.g., cigarette smoke, perfumes, various
chemicals, and other noxious odorants) [1].
Nonallergic, or vasomotor, rhinitis results from dysfunction of the autonomic
nervous system or blood ow changes from iatrogenic or drug-related causes [3].
Increases in blood ow or parasympathetic tone or decreases in the sympathetic
tone increase congestion and drainage of the nasal cavity. Conversely, reduction of
blood ow, suppression of the parasympathetic system, and stimulation of the sympathetic system decrease nasal congestion and discharge. Supplemental female hormones or hormonal changes caused by pregnancy or menstruation may affect nasal
systems. Any medications taken for hypertension or cardiac dysfunction may affect
nasal physiology [1].
Nasal physiology also is affected by anatomic deformities that may have a varying effect on congestion, drainage, and olfaction. Septal deviation and enlarged turbinates can affect airow into the nasal cavity, transforming it from a laminar pattern
to a more turbulent pattern (see the images below). Turbulent airow causes further
irritation to nasal membranes, with a resultant increase in nasal drainage and congestion [1].
3.2 Larynx Anatomy andPhysiology
3.2.1 Larynx Anatomy
3.2.1.1 Cartilages oftheLarynx
Cricoid Cartilage
The cricoid cartilage is a ring of hyaline cartilage located at the inferior aspect of the
larynx and is the only complete ring of cartilage around the trachea. It has the shape
of a “signet ring,” with a broad portion posterior to the airway (lamina of cricoid
cartilage) and a narrower portion circling anteriorly (arch of cricoid cartilage). The
posterior surface of the lamina contains two oval depressions, which serve as attachment sites for the posterior cricoarytenoid muscles, separated by a vertical midline
ridge that serves as an attachment to the esophagus [9].
At the junction of the lamina with the arch, small, round articular facets exist on
the outer posterolateral surface of each side of the ring that articulate with the inferior horn of the thyroid cartilage. The lower border of the cricoid cartilage is connected to the rst tracheal ring by the cricotracheal ligament. The upper border of
the cricoid cartilage gives attachment to the cricothyroid ligament on the anterior

3 Structural andPhysiological Basis oftheUpper Respiratory Tract
39
midline, the cricothyroid muscles on the lateral aspects, and the bases of a pair of
arytenoid cartilages on both sides of the posterior aspect [9].
Thyroid Cartilage
The thyroid cartilage is the largest of the laryngeal cartilages. It is formed by a right
and a left lamina that are separated posteriorly and joined together at an acute angle
in the anterior midline, forming the laryngeal prominence, commonly known as
Adam’s apple. The laryngeal prominence is more apparent in men because the angle
between the two laminae is more acute in men (90°) than in women (120°) [9].
The superior thyroid notch is a V-shaped notch immediately above the laryngeal
prominence, while the inferior thyroid notch is less distinct and located in the midline along the base of the cartilage (see the image below). The two laminae are
quadrilateral in shape and form the lateral surfaces of the thyroid cartilage that
extend obliquely to cover each side of the trachea [9].
The posterior aspect of each lamina is elongated to form a superior horn and an
inferior horn. The medial surfaces of the inferior horns articulate with the outer
posterolateral surface of the cricoid cartilage. The inferior border of the thyroid
cartilage is attached to the cricoid cartilage by the cricothyroid membrane in the
midline and the cricothyroid muscles on either side. The superior horn along with
the entire superior edge of the thyroid cartilage is attached to the hyoid bone by the
thyrohyoid membrane [9].
Epiglottis
The epiglottis is a leaf-shaped cartilage that moves down to form a lid over the glottis and protects the larynx from aspiration of foods or liquids being swallowed. It is
attached by its stem to the midline of the inner aspect of the thyroid cartilage, about
halfway between the angle of the laryngeal prominence and the inferior notch [9].
It is attached via the thyroepiglottic ligament and projects posterosuperiorly to
cover the superior opening of the larynx. The midline of the superior surface of the
epiglottis is also attached to the body of the hyoid bone via the hyoepiglottic ligament. The mucous membrane covering the upper anterior part of the epiglottis
reects off the sides of the epiglottis, giving rise to the glosso-epiglottic folds. The
aryepiglottic folds are mucosal folds on the posterior surface of the epiglottis. The
depressions on either side of the median fold, between the root of the tongue and the
epiglottis, are called the valleculae epiglottica [9].
Arytenoid Cartilages
The arytenoid cartilages form the part of the larynx to which the vocal ligaments
and vocal folds attach. They are pyramidal in shape and have three surfaces, a base,
and an apex. They are located superior to the cricoid cartilage in the posterior part
of the larynx, with the base of the arytenoid cartilages articulating on either side
with the posterior aspect of the upper border of the cricoid lamina. The anterior
angle of the base of the arytenoid cartilage is elongated to form a vocal process for
attachment of the vocal ligament, while the lateral angle is elongated to form a muscular process for attachment of the posterior and lateral cricoarytenoid muscles [9].

40
O. Oğuz et al.
The posterior surface of the arytenoid cartilage gives attachment to the arytenoid
muscle. The anterolateral surface has two depressions for attachment to the false vocal
cord (vestibular ligament) and the vocalis muscle. The medial surface has a mucosal
lining that forms the lateral aspect of the respiratory part of the glottis. The apex of the
arytenoid cartilage is pointed and articulates with the corniculate cartilage [9].
Corniculate Cartilages
The corniculate cartilages are two small, conical cartilages that articulate with the apices of the arytenoid cartilages, serving to extend them posteriorly and medially. They
are located in the posterior parts of the aryepiglottic folds of mucous membrane [9].
Cuneiform Cartilages
The cuneiform cartilages are two small, club-shaped cartilages that lie anterior to the
corniculate cartilages in the aryepiglottic folds. They form small, whitish elevations
on the surface of the mucous membrane just anterior to the arytenoid cartilages [9].
3.2.1.2 Ligaments oftheLarynx
Extrinsic Ligaments
The thyrohyoid membrane is a broad broelastic ligament that spans between the
superior border of the thyroid cartilage and the hyoid bone above. It contains an
aperture on the lateral surfaces of each side for the superior laryngeal arteries,
nerves, and lymphatics [9].
The hyoepiglottic ligament extends from the midline of the superior surface of
the epiglottis to the body of the hyoid bone, located anterosuperiorly. The cricotracheal ligament connects the lower border of the cricoid cartilage to the upper border
of the rst tracheal cartilage ring [9].
Intrinsic Ligaments
The conus elasticus, a submucosal membrane, extends superiorly from the anterior
arch of the cricoid cartilage and attaches to the thyroid cartilage anteriorly and the
vocal processes of the arytenoid cartilages posteriorly. The free superior margin of
the conus elasticus is thickened to form the vocal ligament, which forms the vocal
folds (true vocal cords) once covered by mucosa [9].
The quadrangular membrane, another submucosal sheet, extends between the
lateral aspects of the epiglottis and the anterolateral surface of the arytenoid cartilages on each side. The free lower inferior margin of this membrane is thickened to
form the vestibular ligament, which forms the vestibular folds (false vocal cords)
once covered by mucosa [9].
3.2.1.3 Cavities oftheLarynx
Laryngeal Cavity
The laryngeal central cavity is tubular in shape and lined with mucosa. The superior
aspect of the cavity (laryngeal inlet) opens into the pharynx, inferior and posterior

3 Structural andPhysiological Basis oftheUpper Respiratory Tract
41
to the tongue. The inferior aspect of the cavity is continuous with the lumen of the
trachea [9].
The laryngeal cavity may be divided into three major regions: the vestibule, the
middle, and the infraglottic space. The vestibule is the upper portion of the cavity,
in between the laryngeal inlet and the vestibular folds. The middle portion of the
cavity, or the voice box, is formed by the vestibular folds above and the vocal folds
below. The infraglottic space is the lower portion of the cavity, in between the vocal
folds and the inferior opening of the larynx into the trachea [9].
Laryngeal Ventricles andSaccules
On either side of the middle laryngeal cavity, between the vestibular and vocal
folds, the mucosa bulges laterally to form troughs known as the laryngeal ventricles.
The laryngeal saccules are tubular extensions of each ventricle anterosuperiorly
between the vestibular fold and the thyroid cartilage. It is thought that the walls of
these saccules contain many mucous glands that lubricate the vocal folds [9].
Rima Vestibuli andRima Glottidis
The rima vestibuli is the triangular-shaped opening between the two adjacent vestibular folds. The apex lies anterior and the base is formed by the posterior wall of
the laryngeal cavity. The rima glottidis is a narrower, triangular-shaped opening that
lies beneath the rima vestibuli, formed by the two adjacent vocal folds [9].
Piriform Recesses
The piriform recesses (piriform sinuses) are present on either side of the anterolateral wall of the laryngopharynx. They are bounded medially by the aryepiglottic
folds and laterally by the thyroid cartilage and thyrohyoid membrane. They are a
common place for food to become trapped [9].
3.2.1.4 Muscles oftheLarynx
Cricothyroid Muscles
The cricothyroid muscles are attached to the anterolateral surfaces of the arch of the
cricoid cartilage and expand superiorly and posteriorly to attach to the inferior border of the thyroid cartilage. They are the only laryngeal muscles supplied by the
external branch of the superior laryngeal nerve, a branch of the vagus nerve (cranial
nerve [CN] X) below the base of the skull [9].
These muscles function to elevate the anterior arch of the cricoid cartilage and
depress the posterior portion of the thyroid cartilage lamina. This produces tension
and elongation of the vocal cords, resulting in higher-pitch phonation [9].
Posterior Cricoarytenoid Muscles
The posterior cricoarytenoid muscles extend from the oval depressions on the posterior surface of the cricoid lamina on each side and extend upward to the muscular
process of the arytenoid cartilage on the same side. These muscles function to rotate
the arytenoid cartilages laterally, thereby abducting the vocal cords. Their action
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