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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
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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)

240
A. Türkcan et al.
identied by the intricate binding pattern they generate. It is safe to assume the same
holds for people. It is fascinating that these genes have been found in unexpected
places, including sperm and the digestive tract. Researchers are trying to gure out
what these genes do besides aid with smell [8].
When an odorant connects to a receptor, a signaling cascade causes the neuron to
depolarize and convey the signal along the neuron’s axon. These axons eventually
converge within the la olfactory, a bundle of axons that extends deep into the epithelium [5].
These axons go ipsilaterally to the olfactory bulb via the cribriform plate. The
olfactory receptor cells communicate with mitral and tufted cells in the olfactory
bulb, clustered in glomeruli structures. Receptor-like neurons generate an early
topographical odorant map by having their axon terminals connect inside the same
glomeruli. The chemical makeup of an odor is assumed to trigger a specic set of
odorant receptors. In response, the olfactory bulb’s associated glomeruli get excited,
resulting in a distinct excitation pattern for each odorant [5].
The olfactory bulb’s central transmitter neurons are the glomerular cells. Axons
from these cells travel to the olfactory cortex, which is divided into ve parts,
including [1] the anterior olfactory nucleus, connecting the two olfactory bulbs
through the anterior commissure, [2] the olfactory tubercle, [3] the pyriform cortex,
which is the central olfactory discrimination region, [4] the cortical nucleus of the
amygdala, and [5] the entorhinal area, which projects to the hippocampus [5].
No thalamic relay is required for the olfactory pathway’s cortical projections to
occur. The conscious experience of scents likely involves relays from the olfactory
tubercle and the pyriform cortex, which project to other olfactory cortical areas and
the medial dorsal nucleus of the thalamus [5].
On the other hand, the limbic system’s entorhinal region and the amygdala’s
cortical nucleus may have a role in the hedonic or emotional aspects of smells.
When a highly unpleasant odorant is introduced, regional cerebral blood ow (as
assessed by positron emission tomography) increases dramatically in the amygdala,
and this rise is correlated with subjective assessments of perceived aversiveness [5].
The vomeronasal organ (VNO), or the Jacobson organ, is a membrane structure
found on both sides of the nose, nestled deep inside the nasal respiratory mucosa
and close to the septal perichondria. When the septal cartilage meets the bony septum, 2cm from the nose, its opening may be seen in the nasal vestibule in 91–97%
of adult individuals. Postnatal humans have not been discovered to have axons
extending from the VNO [5], as seen in lower species.
18.4 Odor Threshold Tests
Odor threshold studies use the progressive presentation of phenyl ethyl alcohol or
n-butanol probes at varying concentrations, sometimes in combination with odorless probes (“blanks”) [2, 3]. Patients are required to respond (= forced-choice process) [2] even if they are unsure about whether or not they have experienced an odor.
Once the threshold for detecting the odor probe has been crossed, the odor concentration gradually declines and increases throughout several iterations [3]. By

18 Smell Testing: Purpose, Procedure, Interpretation
averaging the reversals, as is done here, dependability is improved [3]. The Snap
and Sniff [9] and the pen-like odor dispensing device [10] threshold tests are often
employed in clinical practice.
241
18.5 Tests ofSmell Sensitivity Above theThreshold
Suprathreshold testing employs patient-perceivable doses of odorants. The University
of Pennsylvania Smell Identication Test (UPSIT) and odor identication tests using
pen-like odor dispensing devices [11, 12] are the most frequently utilized suprathresh-
old tests. The forced-choice approach involves providing the patient with a list of
possible responses in written or visual form and then having them smell an odor probe
and select the one they believe is correct. The test’s outcome is reported as the total
number of correct responses. Due to cultural differences, the validity and reliability of
the reported scents must be veried for each community studied [3]. Most of these
exams come with normative data that may be used to place a person in a percentile
range based on their gender and age [2, 3]. Odor discrimination tests, such as those
done using pens that dispense odors, are another type of suprathreshold test. The
patient is given a series of odor probes and instructed to memorize and discriminate
between them; however, they are not required to provide particular names to the scents
they smell. Once again, the test’s outcome is recorded as the total number of correct
responses. Compared to olfactory threshold testing, suprathreshold tests need higher
levels of cognitive capacity, namely in executive function and semantic memory [13].
Hedonic value tests are another kind of suprathreshold olfactory test [2, 3]. These
procedures incorporate emotional factors since they determine whether or not a specic
odor is liked or disliked. In the medical eld, hedonic tests are infrequently used [1].
18.6 Tests toDetermine Gustatory Abilities
When patients experience a loss of smell, they typically also experience a loss of
taste [2, 3]. This is because the retronasal pathway allows volatiles from meals to
reach the olfactory receptors and trigger the olfactory receptors on the olfactory
epithelium. Smells associated with food are misinterpreted as “taste,” even when
gustatory skill is unaffected. So, screening for gustatory functioning, including liquids applied to the tongue or the taste strip test [14, 15], should be a part of olfactory
testing. The patient is asked to report if the probe feels salty, sour, bitter, or sweet
when it is dropped or placed on the tongue. The score on the exam is determined by
the total number of correct responses [1].
18.7 Personal Evaluation ofSmell
The inuence of olfactory cues (or the lack thereof) on our actions may not always
be evident [2, 3]. Furthermore, patient self-assessments are negatively associated
with objective tests of their sense of smell [16, 17]. However, a scale from zero

242
(none) to ten (superb) may be employed for subjective reporting of olfactory abilities, such as in epidemiological investigations [18].
A. Türkcan et al.
18.8 Clinical Measurement ofOlfaction
When chemosensory dysfunction is the primary complaint, it is crucial to quantify
the degree to which smell and taste are impaired. Sensory testing is performed primarily to evaluate chemosensory impairment [5].
Some commercially accessible tests aim to standardize and streamline the arduous clinical examination process. Testing one nostril at a time may be more successful in detecting an olfactory disease [19], even though it is common practice to test
both simultaneously to save time. This is in contrast to other sensory systems, where
testing in just one direction is routine for identifying pathology.
There are now olfactory function tests available that can evaluate a person’s
olfactory capacity by gauging their threshold for detecting and identifying odors.
The butanol threshold test (Sensonics, Inc., www.sensonics.com), the University of
Pennsylvania Smell Identication Test (UPSIT), and the Snifn’ Sticks test
(Burghart Messtechnik GmbH, www.burghart- mt.de) are also examples of such
assessments. Odor recognition tests and electrocorticographic (ECoG) measurements of the brain have been utilized in laboratories to assess abnormal smell in
patients with neurological disorders [5].
18.8.1 Butanol Threshold Test
The butanol threshold test is a forced-choice procedure wherein one sniff vial contains an aqueous concentration of butyl alcohol, and the other has water. The patient
is asked to choose which bottle contains the odorant; this is done independently for
each nostril. If they get even one of the choices wrong, the concentration of butanol
in the bottle is increased by a factor of 3, and so on, until they either get ve answers
right or are unable to choose the bottle containing 4% butanol.
The detection threshold is the lowest butanol concentration at which the patient
responded afrmatively on ve occasions. The patient’s point is compared to that of
a normative sample of subjects using the scoring system [5].
18.8.1.1 The Penn State University Odor Identification Exam
The UPSIT uses a scratch-and-sniff style with 40 microencapsulated scents and
four different response options. The individual is given the exam alone and told to
make an educated estimate if they get a question wrong [5].
Patients with anosmia often have a 10% accurate rate or lower (10/40). The data
is examined by comparing the test results to age- and gender-specic norms. The
reliability of this exam across administrations is relatively high [5].
A table compares scores from different patient groups, such as those with multiple sclerosis, those with Korsakoff syndrome, and those pretending to have

18 Smell Testing: Purpose, Procedure, Interpretation
anosmia. Those in the second category routinely post-test scores much below what
would be predicted by random chance [5].
243
18.8.2 Cross-Cultural Smell Identification Test
A UPSIT variation that may be administered in 5min was proposed for a speedy
evaluation of smell. Input on odor recognition from several cultures went into creating the Cross-Cultural Smell Identication Test (CC-SIT), which consists of 12
items. These nations include China, Colombia, France, Germany, Italy, Japan,
Russia, and Sweden.
Bananas, chocolate, cinnamon, gasoline, lemon, onion, paint thinner, pineapple, rose, soap, smoke, and turpentine are some of the odorants that may be
found. Representatives from all countries most commonly detected these odorants [5].
Due to its speed and accuracy, this test is an excellent replacement for more timeconsuming methods of assessing olfactory function in a clinical context.
The short duration of the test reduces its ability to pick up on small shifts in
olfactory function [5].
18.8.3 Sniffin’ Sticks
Three aspects of smell are tested using a set of reusable pens with built-in odor
dispensers: (1) odor threshold using a single staircase method, (2) odor discrimination using forced choice between 3 of 16 commonly used odorants, and (3) odor
identication using multiple forced choice from four verbal items. To get a complete picture of how well your sense of smell is working, add up your scores from
all three tests to get a total score out of 5.
18.8.4 Olfactory-Evoked Response (Usually Reserved
forResearch Studies)
Electrodes placed on the scalp (EEG) and the eye (electrooculogram) measure
olfactory-evoked potentials, normalizing the patient’s sensitivity to eye movements.
Maintaining focus requires a visual tracking job, but white noise played through
headphones covers up any audible cues [5, 6].
Carbon dioxide (which has no smell but stimulates the trigeminal nerve) or
hydrogen sulde is supplied to the nose in a steady stream via an olfactometer. The
initial negative peak, denoted by N1, is followed by a second positive trough, represented by P2. These two numbers (both 5) are used to calculate latencies.
The clinical use of olfactory evoked responses as a standard diagnostic tool is
limited. The UPSIT outperformed olfactory evoked responses in identifying abnormalities in individuals with neurologic illness [5].

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A. Türkcan et al.
The authors have shown that the self-administered UPSIT test helps measure
olfactory function in a busy clinical practice. A simple screening test with a typical
alcohol pad can be performed instead if the olfactory tests mentioned above are
unavailable. The patient is given the contents of the envelope after opening it. The
pad is placed at the level of the umbilicus and is gradually pushed closer to the nose
while the patient’s eyes are closed. The patient must let the tester know when alcohol is discovered again. Patients with hyposmia [5] can be identied by a pad placement less than 20cm from their nose.
References
1. Kronenbuerger M, Pilgramm M. Olfactory testing. In: StatPearls. Treasure Island, FL:
StatPearls Publishing; 2023. https://www.ncbi.nlm.nih.gov/books/NBK565861/. Accessed 23
Oct 2023.
2. Hummel T, Whitcroft KL, Andrews P, Altundag A, Cinghi C, Costanzo RM, Damm M, Frasnelli
J, Gudziol H, Gupta N, Haehner A, Holbrook E, Hong SC, Hornung D, Hüttenbrink KB, Kamel
R, Kobayashi M, Konstantinidis I, Landis BN, Leopold DA, Macchi A, Miwa T, Moesges R,
Mullol J, Mueller CA, Ottaviano G, Passali GC, Philpott C, Pinto JM, Ramakrishnan VJ,
Rombaux P, Roth Y, Schlosser RA, Shu B, Soler G, Stjärne P, Stuck BA, Vodicka J, WelgeLuessen A.Position paper on olfactory dysfunction. Rhinology. 2016;56(1):1–30.
3. Doty RL. Psychophysical testing of smell and taste function. Handb Clin Neurol.
2019;164:229–46.
4. Whitcroft KL, Cuevas M, Haehner A, Hummel T.Patterns of olfactory impairment reect
underlying disease etiology. Laryngoscope. 2017;127(2):291–5.
5. Holbrook EH.Disorders of taste and smell. In: Meyers AD editor. Medscape. 2022. https://
emedicine.medscape.com/article/861242- overview#a4. Accessed 23 Oct 2023.
6. Tuccori M, Lapi F, Testi A, Ruggiero E, Moretti U, Vannacci A, etal. Drug-induced taste and
smell alterations: a case/non-case evaluation of an Italian database of spontaneous adverse
drug reaction reporting. Drug Saf. 2011;34(10):849–59.
7. Schwob JE, Jang W, Holbrook EH, Lin B, Herrick DB, Peterson JN, et al. Stem and progenitor cells of the mammalian olfactory epithelium: taking Poietic license. J Comp Neurol.
2017;525(4):1034–54.
8. Patel RM, Pinto JM.Olfaction: anatomy, physiology, and disease. Clin Anat. 2014;27(1):54–60.
9. Doty RL, Wylie C, Potter M, Beston R, Cope B, Majam K.Clinical validation of the olfactory
detection threshold module of the Snap & Sniff® olfactory test system. Int Forum Allergy
Rhinol. 2019;9(9):986–92.
10. Hummel T, Sekinger B, Wolf SR, Pauli E, Kobal G. ‘Snifn’ sticks’: olfactory performance
assessed by the combined testing of odor identication, odor discrimination and olfactory
threshold. Chem Senses. 1997;22(1):39–52.
11. Doty RL, Shaman P, Dann M. Development of the University of Pennsylvania Smell
Identication Test: a standardized microencapsulated test of olfactory function. Physiol Behav.
1984;32(3):489–502.
12. Kobal G, Hummel T, Sekinger B, Barz S, Roscher S, Wolf S. “Snifn’ sticks”: screening of
olfactory performance. Rhinology. 1996;34(4):222–6.
13. Hedner M, Larsson M, Arnold N, Zucco GM, Hummel T. Cognitive factors in odor
detection, odor discrimination, and odor identication tasks. J Clin Exp Neuropsychol.
2010;32(10):1062–7.
14. Hummel T, Landis BN, Hüttenbrink KB. Smell and taste disorders. GMS Curr Top
Otorhinolaryngol Head Neck Surg. 2011;10:Doc04.

18 Smell Testing: Purpose, Procedure, Interpretation
15. Mueller C, Kallert S, Renner B, Stiassny K, Temmel AF, Hummel T, Kobal G.Quantitative
assessment of gustatory function in a clinical context using impregnated “taste strips”.
Rhinology. 2003;41(1):2–6.
16. Adams DR, Wroblewski KE, Kern DW, Kozloski MJ, Dale W, McClintock MK, Pinto
JM. Factors associated with inaccurate self-reporting of olfactory dysfunction in older US
adults. Chem Senses. 2017;42(3):223–31.
17. Nordin S, Monsch AU, Murphy C.Unawareness of smell loss in normal aging and Alzheimer’s
disease: discrepancy between self-reported and diagnosed smell sensitivity. J Gerontol B
Psychol Sci Soc Sci. 1995;50(4):P187–92.
18. Hoffman HJ, Ishii EK, MacTurk RH.Age-related changes in the prevalence of smell/taste
problems among the United States adult population. Results of the 1994 disability supplement
to the National Health Interview Survey (NHIS). Ann N Y Acad Sci. 1998;855:716–22.
19. Poupon D, Hummel T, Haehner A, Welge-Luessen A, Frasnelli J.Nostril differences in the
olfactory performance in health and disease. Chem Senses. 2017;42(8):625–34.
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Taste Testing: Purpose, Procedure, Interpretation
RamazanÖcal, NurayBayar Muluk, andDesiderioPassali
19.1 Introduction
Several factors can contribute to adult taste and smell disorders, including metabolic
and endocrine abnormalities, neurological disorders, inammatory conditions of
the nasal passages and paranasal sinuses, head trauma and surgery, infections,
chemical exposures, medications, and normal aging. Flavor perception can be signicantly impacted by problems with taste and smell, which can lower quality of
life and make it difcult to obtain enough nourishment [1].
19.2 Definitions
19
Normogeusia and normosmia relate to having typical gustatory and olfactory capabilities. Flavor and odor problems include [1].
19.2.1 Taste Dysfunction Abnormalities
Disturbances of taste perception include the following:
R. Öcal
Department of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Ankara
Research and Training Hospital, Health Sciences University, Ankara, Türkiye
N. Bayar Muluk (*)
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, Türkiye
D. Passali
Department of Medical, Surgical and Neuroscience Sciences, and Department of
Otorhinolaryngology, University of Siena, Siena, Italy
© 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_19
247

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R. Öcal et al.
• Hypogeusia, in which something that would generally taste good feels bad;
• Ageusia, in which taste function is absent;
• Dysgeusia, in which taste sensations (of sweetness, sourness, saltiness, bitter-
ness, or metallicity) change in response to a tastant stimulus.
• Aliageusia, in which something that would typically taste good feels bad;
• Parosmia, Abhorrent odor perception either with an odorant stimulus (troposmia
or smell distortion) or without an odorant stimulus (phantosmia).
• Dysosmia is a general term for abnormalities in olfactory perception.
It includes conditions such as hyposmia (reduced smell function) and anosmia
(the inability to detect odors), as well as parosmia (the perception of unpleasant
odors in response to an odorant stimulus (troposmia or smell distortion) or in the
absence of such a stimulus (phantosmia)).
19.3 Anatomy andPhysiology ofTaste
Different receptors and cerebral pathways are involved in gustation and olfaction,
respectively; hence, their physiology and anatomy are distinct. Efferent taste, olfactory input, and other sensory data are necessary for accurate avor perception [1].
The sense of taste is triggered when a chemical or other stimulus activates taste
receptor cells, sending signals to the brain via afferent nerves [1].
Information regarding tastants (taste-stimulating chemicals or substances) is
received by taste receptor cells (neuroepithelial cells) and transmitted to the central
nervous system via afferent neurons. The typical lifespan of a taste receptor cell is
10days [2].
The tongue’s dorsal and lateral surfaces, as well as the soft palate, uvula, larynx,
pharynx, epiglottis, and esophagus [3], are home to taste buds, each of which contains approximately 50–150 taste receptor cells. Taste pores, tiny apertures in the
epithelial surface, are how tastants travel to the receptor cells within the taste buds.
Papillae are the structures that house taste buds on the tongue. The three types of
papillae are as follows [1]:
The fungiform papillae can be seen throughout the rst two-thirds of the tongue.
The average number of papillae on a human tongue is 190, although this can range
from 184 to 198. Eighty percent of the tongue’s fungiform taste buds are found in
the rst 2cm [4].
The tongue’s foliate papillae are found on its dorsal and lateral posterior surfaces.
These papillae, known as the circumvallate papillae, are found toward the back
of the tongue.
Twenty taste buds are packed into each fungiform papillae, whereas hundreds are
packed into each circumvallate and foliate papillae [5].
The vagus nerve (cranial nerve X), glossopharyngeal nerve (cranial nerve IX),
and facial nerve (cranial nerve VII) all provide innervation to areas of the brain that
contain taste buds [1].

19 Taste Testing: Purpose, Procedure, Interpretation
249
The chorda tympani is a branch of the facial nerve that supplies sensation to the
front two-thirds of the tongue. The supercial petrosal nerve, another facial nerve
branch, provides feeling to the palate.
The glossopharyngeal nerve supplies the back of the tongue with sensation.
The vagus nerve supplies the vocal cords and pharynx.
The solitary tract nucleus in the medulla is the site of synaptic connections made
by primary afferent taste neurons. The primary gustatory cortex and thalamus
receive taste information [6]. Due to the involvement of numerous cranial nerves in
gustatory function [1], ageusia (total loss of taste) cases are sporadic.
The subjective gustation experience is inuenced by more than just the afferent
taste innervation of the tongue and taste buds. Other sensations, such as the burning
and irritation given by hot peppers and the odors of ammonia, are accounted for by
the branches of the trigeminal nerve (cranial nerve V), which innervate the inside of
the mouth and nasal cavities. The nasal cavity and oropharynx are also supplied
with sensory nerves from the anterior ethmoid, nasopalatine, posterior palatine, and
buccal regions [1].
The tastants must pass through the mucous layer above the taste receptor neurons, and saliva plays a crucial part in this process. Water-soluble taste chemicals
are easily transported to receptor cells, but insoluble tastants require carrier proteins [1].
By activating protein-coupled receptors, tastant administration leads to membrane alterations that open ion channels and neuron depolarization [7].
If there is an aberration in any of these components, it might lead to alterations
in gustatory function. Causes of aberrant taste include abnormalities in the taste cell
receptor proteins or ion channels [8–10] and changes in the makeup of saliva or
mucous around the taste buds [11–14].
Sweet, sour, salty, and bitter are the four traditional taste qualities mentioned and
commonly evaluated. In addition, umami (the glutamate taste) is discussed [15–17].
Due to the intricacy of the umami taste system, it has traditionally been more practical to examine only the original four taste qualities; however, umami is sometimes
included in regular clinical evaluations of gustatory function [1].
19.4 Etiology ofGustatory Dysfunction
Many things that people think are avor aws are, in fact, the result of a problem
with their sense of smell. The avor is a multisensory experience originating from
the food’s aroma, taste, texture, and warmth. When food is introduced to the mouth,
it stimulates several different taste buds [18].
Tongue movement can help spread the avor over more taste buds, improving the
overall avor. Taste is the sense that adaptation has the most signicant impact [18].
Taste dysfunction can have various causes, but the most common causes include
a previous upper respiratory tract infection (URTI), a head injury, or idiopathic causes.

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Impairment of gustation can be caused by damage to any part of the gustatory
system, including the mucosa, taste buds, unmyelinated nerves, cranial nerves, or
the brain stem [18].
Disorders of the oral cavity and mucosa, such as infections, inammation, and
radiation-induced mucositis, can diminish the ability to taste. Since taste buds are
typically considered radioresistant [18], the microvilli of the taste buds are likely to
be the site of harm during irradiation.
Hypogeusia and cacogeusia are often the result of neglectful dental care.
Secondary taste bud involvement is a potential cause of taste abnormalities caused
by infections with viruses, bacteria, fungi, and parasites [18].
It is not the loss of taste buds that causes average aging-related taste loss [19, 20]
but alterations in taste cell membranes, including altered activity of ion channels
and receptors.
Over two hundred drugs [21] have been linked to impaired taste. This is especially important for clinicians to remember when dealing with patients taking many
medications.
Loss of appetite and loss of taste bud function are common side effects of head
and neck cancer treatment [18].
Dentures and other palatal prostheses can reduce your ability to detect sour and
bitter avors, and cleaning your tongue can dull your sense of taste [18].
Taste can be temporarily or permanently altered through surgery. When the
tongue or other parts of the mouth are removed, most often for cancer treatment,
the number of taste buds in the mouth is reduced. Chemotherapy and radiation
can impair one’s sense of taste by damaging taste receptors and reducing saliva
production. Temporary dysgeusia can occur after otologic surgery if the chorda
tympani nerve is stretched or cut. Alternate innervation from the otic ganglion
to the geniculate ganglion via the more signicant supercial petrosal nerve
[18] means that even a bilateral injury may not produce permanent taste
abnormalities.
The senses of smell and taste could be negatively affected by gastric bypass. A
total of 73% and 42% of 103 patients in a study by Graham etal. who underwent
Roux-en-Y gastric bypass reported changes in taste and smell, respectively [3]. In
contrast, patients appear to have less olfactory loss if the bypass is performed laparoscopically [22].
Flavor deviations are associated with nutritional decits. Reduced amounts of
zinc, copper, and nickel have been linked to unpleasant taste sensations. Anorexia,
malabsorption, and excessive urine loss contribute to nutritional decits [18].
Taste and olfactory abnormalities are often linked to endocrine issues. Sensitivity
to taste may be diminished by diabetes mellitus, hypogonadism, Sjögren syndrome,
and pseudohypoparathyroidism and enhanced by hypothyroidism and adrenal cortical insufciency. Taste is also affected by hormonal shifts during menstruation and
pregnancy [18].
A more signicant detection threshold for glutamic acid and hydrochloride is
observed in AIDS patients [23], and AIDS patients frequently report changes in
their sense of taste.
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