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M.S. DEGREE EXAMINATION Branch IV – E.N.T. (For candidates admitted from 2004-2005 to 2008-2009 onwards) Paper I – APPLIED BASIC SCIENCES IN OTO RHINOLARYNGOLOGY
I. ANATOMY – Answer any FOUR: (4 x 5 = 20) 1. Pyriform fossa. It is a potential space that lies on either side of the larynx. They are two in number. It is shaped like a pyramid with the base pointing above and the apex below. They belong to the hypopharyngeal area of the pharynx. It has two parts; the shallow upper part and a deeper lower part.
Boundaries: The pyriform fossa is bounded laterally by the mucosa covering the lamina of the thyroid cartilage. Medially it is bounded by the aryepiglottic fold and arytenoid cartilages above and the cricoid cartilage below. Superiorly it is bounded by the lateral glosso epilglottic fold (Pharyngoepiglottic fold), inferiorly it continues with the oesophagus.
Deep to the mucous membrane of the lateral wall of the pyriform fossa lies the internal laryngeal branch of the superior laryngeal nerve. It supplies sensori fibres to this area.
Clinical importance of pyriform fossa: 1. Anatomically it is a hidden area. Any malignancy in this area will initially cause fewer symptoms and has a tendency to present very late. 2. This area is richly endowed with lymphatics. They drain into the upper deep cervical group of lymph nodes. Any malignancy in this area has a tendency for nodal metastasis. 3. Foreign bodies in the throat commonly get lodged here. 4. Since superior laryngeal nerve lies superficially in this area, it can be topically blocked by placing cotton plegets soaked in 4% xylocaine in this area. This is known as the pyriform fossa block.
Examination of the pyriform fossa: The superficial shallow portion of the pyriform fossa is easily visible in a laryngeal mirror. This portion will be visible in the indirect laryngoscopy examination. The deeper portion of the pyriform fossa is hidden and is not visible to the IDL mirror. Only a direct examination using a upper oesophageal speculum will reveal this portion. Tumors involving the pyriform fossa commonly arise from its deep portion. This may escape detection during a IDL scopy examination. But if one looks for pooling of saliva in the involved pyriform fossa the underlying growth can be suspected. Hence pooling of saliva is an important clinical sign indicating a under lying tumor in the deep portion of the pyriform fossa, or the presence of a foreign body can also be suspected by this sign. Causes for pooling of saliva in the pyriform fossa:
Pooling of saliva in the pyriform fossa is not only caused by growth affecting this area causing obstruction to saliva being swallowed, but also due to intense cricopharyngeal muscle spasm. 1. Malignant growth involving the deep portion of the pyriform fossa 2. Foreign body being lodged in the pyriform fossa. 3. Growth involving the crico pharynx or upper oesophagus can also cause pooling of saliva.
2. Sphenoid sinus.
Sphenoid sinus is located in the skull base at the junction of the anterior and middle cranial fossa. Pneumatisation of sphenoid starts during the 4th year of childhood and gets completed by the 17th year. The sphenoid sinuses vary in size and may be asymmetric. They drain through the superior meatus via a small ostium about 4mm in diameter located disadvantageously 20mm above the sinus floor. This sinus is related to several important vital structures. They are: 1. Pituitary gland lies above the sphenoid sinus. 2. Optic nerve and internal carotid arteries traverse its lateral wall. 3. The nerve of pterygoid canal lies in the floor of the sinus. Hence infections of sphenoid sinus may involve the optic nerve if the canal of the optic nerve is dehiscent.
Figure showing sphenoid sinus Pneumatization of sphenoid sinus is highly variable the knowledge of which is important in surgeries involving this sinus. Depending on the extent of pneumatization it is classified into three types: Conchal type:
Conchal type pneumatization This type of pneumatization is common in children under the age of 12 because pneumatization of this sinus begins to develop after the age of 12. In this type of sphenoid sinus the area below the sella is a solid block of bone without an air cavity.
Presellar type of pneumatization: In this type the air cavity does not penetrate beyond the coronal plane defined by the anterior sellar wall.
Sellar type: In this type the air cavity extends into the body of sphenoid below the sella and may extend as far posteriorly as the clivus. This type of pneumatization is seen in more than 80% individuals.
Ostium of sphenoid sinus is located in the sphenoethmoidal recess. It is commonly seen medial to the superior turbinate about 1.5 cms superior to the posterior choana. It lies just a few millimetres below the cribriform plate. The right and left sphenoid sinus are separated by an intersinus septum. The position and attachment of this septum is highly variable. Possible variations of sphenoidal septum include: 1. Single intersinus septum extending on to the anterior wall of sella 2. Multiple incomplete septa may be seen 3. Accessory septa may be present. These could be seen terminating in the optic nerve / internal carotid artery To avoid damaging optic nerve / carotid artery it should be removed by nibbling with true cut forceps during surgical procedures involving sphenoid sinus. Lateral wall of sphenoid sinus is related to cavernous sinus. Cavernous sinus is usually formed by splitting of dura. This sinus extends from the orbital apex to the posterior clinoid process. This sinus contains delicate venous channels, cavernous portion of internal carotid artery, 3, 4, 6 cranial nerves and variable amounts of fatty tissue. The prominence of internal carotid artery lies in the postero lateral aspect of the lateral wall of sphenoid sinus. This prominence is well identified in well pneumatised sphenoid sinuses. In the anterior superior aspect of the lateral wall is seen the bulge of the optic nerve caused by the underlying optic nerve. These two prominences are separated by a small dimple known as the optico carotid recess. The optic nerve and internal carotid artery are separated from the sphenoid sinus by a thin piece of bone. Sometimes this bone may even be deficient leaving them naked within the sinus cavity. In well pneumatised sphenoid sinuses the pterygoid canal and a portion of the maxillary division of trigeminal nerve could be seen in their lateral recess. The roof of the sphenoid is continuous with that of ethmoid sinus anteriorly and this area is known as planum sphenoidale. At the junction of the roof and posterior wall the bone of sphenoid sinus is thickened to form the tuberculum sella. Inferior to tuberculum sella in the posterior wall is the sella turcia. It usually forms a bulge in the midline. The bone over the sella is just 0.5 – 1 mm thick. It is the thinnest in its lower portion and is easy to breach here. It is this area that is opened during endoscopic hypophysectomy. During surgery this area can easily be identified by its bluish tinge which is caused by the underlying dura.
3. Eustachian tube. Synonyms: Pharyngotympanic tube, middle ear ventilating tube
In adults it lies at an angle of 45 degrees to the horizontal plane. In infants this inclination is about 10 degrees. In adults its length is 38mm. For descriptive purposes it can be divided into posterior 1/3 which is osseous in nature and anterior 2/3 which is cartilaginous in nature. Differences between infants and adults: The Eustachian tube is different in infants and adults. These differences include: In infants it is shorter Straighter Wider. Infections from nasopharynx can easily reach the middle ear cavity in infants rather easily. Osseous portion: The osseous portion of the Eustachian tube also known as protympanum lies completely within the petrous portion of the temporal bone. The lumen of the osseus portion of the Eustachian tube is triangular and is open. This is in contrast to that of the cartilaginous portion which is closed at rest. Cartilaginous portion: This portion of the Eustachian tube is longer than that of the osseous portion. This portion is closed at rest and opens during swallowing or during a valsalva manoeuvre. The cartilaginous tube courses antero medially and inferiorly, angled between 30 and 40 degrees. The cartilaginous portion of the tube is not completely surrounded by cartilage, but is deficient infero laterally where it is covered by a membrane. The cartilage is crook shaped covering the medial, lateral and superior walls of the cartilaginous portion of the tube.
This bony cartilaginous tube connects the middle ear to the nasopharynx.
The tubal lumen is shaped like two cones joined at their apices. The junction of the cones is the narrowest portion of the lumen and is known as the isthmus, and is usually situated at the junction of the cartilaginous and bony portion of the tube.
The cartilaginous portion of the Eustachian tube does not follow a straight course in the adult but extends along a curve from the junction of the osseous and cartilaginous portions to the medial pterygoid plate, approximating the skull base during most of its course. The Eustachian tube crosses the superior border of the superior constrictor muscle to enter the nasopharynx. The medial cartilaginous portion of the tube presses against the pharyngeal wall to form a prominent fold, the torus tubaris. The torus is the site of origin of the salpingopalatine and salpingopharyngeal muscles.
The mucosal lining of the Eustachian tube is continuous with that of the nasopharynx and middle ear (ciliated columnar epithelium). Certain differences in the mucosal lining is evident, mucous glands predominate at the nasopharyngeal orifice, and this gradually changes into a mixture of goblet cells at the tympanum. Muscles associated with Eustachian tube: The muscles associated with the Eustachian tube are 4 in number. They are tensor veli palatini, levator veli palatini, salpingopharyngeus, and tensor tympani. Usually the Eustachian tube is closed; it opens during such actions like swallowing, yawning thus equalising the middle ear pressure. Active dilatation of the tube is induced by the tensor veli palatini muscle. Closure of the tube has been
attributed to passive reapproximation of tubal walls by extrinsic forces exerted by surrounding elastic fibres. Blood supply: The Eustachian tube is supplied by the ascending palatine artery, pharyngeal branch of internal maxillary artery, the artery of the pterygoid canal, ascending pharyngeal artery, and the middle meningeal artery. The venous drainage is via the pterygoid plexus. Nerve supply: The pharyngeal orifice of the Eustachian tube is supplied by a branch from the otic ganglion, the sphenopalatine nerve, and the pharyngeal plexus. The reminder of the tube receives its sensory supply from the tympanic plexus and the pharyngeal plexus. The glossopharyngeal nerve has an important role in the innervation of the Eustachian tube. Functions of Eustachian tube: 1. Ventilation 2. Protection 3. Drainage
4. Neck spaces. These spaces are present in the neck between the layers of cervical fascia. These spaces are important from the point of view of clinician because of the propensity of infections to involve this space and to spread along these spaces to involve other areas like the mediastinum. Many of these spaces could as well be inconsequential. There are two types of fascial spaces in the neck. I. Those associated with muscles II. Those associated with viscera and vessels Fascial spaces associated with muscles are limited by the insertion of muscles to bones. These muscular insertions serve as a limiting factor to spread of infections from these spaces. Spaces associated with viscera and blood vessels are not limited by insertion of muscles and hence infections cross and travel long distances if these spaces are involved. Visceral spaces: Lateral pharyngeal space: (Para pharyngeal space) This space is situated lateral to the fascia covering the constrictor muscles of the pharynx (buccopharyngeal fascia). Lateral to this space lie the pterygoid muscle, mandible and carotid sheath. Superiorly it extends up to the skull base while inferiorly it ends at the level of hyoid bone because of the attachment of the submandibular gland sheath to the sheaths of the stylohyoid muscle and the posterior belly of digastric muscle. The carotid sheath lies close to the posterolateral wall of this space. Postero medially this space communicates with the retropharyngeal space. Anteriorly and inferiorly this space communicates with the spaces associated with the floor of the mouth. This space is most commonly involved in neck space infections. Infections from this space can easily spread to the carotid and retropharyngeal spaces. Common routes of infections of parapharyngeal space: 1. Lingual infections 2. Submandibular gland infections 3. Infections involving the parotid space 4. Spread from peritonsillar abscess
Figure showing parapharyngeal space
Diagram showing carotid space Submandibular space: This is actually a combination of two spaces partially separated by the mylohyoid muscle. The space below the mylohyoid muscle is known as the submaxillary space while the space above the muscle is known as sublingual space.
Boundaries: Superior – Oral mucosa and tongue Medial – oral mucosa and tongue Lateral – Superficial layer of deep cervical fascia with its tight attachment to the mandible and hyoid bone laterally Inferior – Hyoid bone The mylohyoid cleft separates the submaxillary from sublingual space. Structures passing through mylohyoid cleft include: 1. Wharton’s duct 2. Lingual nerve 3. Hypoglossal nerve 4. Branch of facial artery 5. Lymphatics There is free communication across midline between these spaces. Ludwig’s angina is the characteristic example of infections of this space.
Masticator space: This space is formed by the splitting of the superficial layer of deep cervical fascia as it encloses the mandible and the primary muscles of mastication. Contents of this space include: 1. Masseter muscle 2. Medial & lateral pterygoid muscles 3. Ramus & posterior portion of the body of mandible 4. Insertion of the temporalis muscle Supero medially this space communicates with the temporal space medial to the zygomatic arch. Infections involving this space involve the temporal space also. The most common cause of infection within this space is from abscessed third molar tooth.
Figure showing masticator space Retropharyngeal space: This space lies between the deep layer of the deep cervical fascia (prevertebral fascia) and the buccopharyngeal fascia superiorly and the fascia covering the oesophagus inferiorly. An ancillary portion of deep cervical fascia referred to as the alar layer extends from the base of skull to approximately the second thoracic vertebra at which point it fuses with that of the fascial covering of the oesophagus. The prevertebral fascia lies over the vertebra and the paraspinal muscles running from the base of the skull to the diaphragm. Thus there are two potential spaces in the retropharyngeal space. The first one lies between the fascia covering the pharynx and oesophagus and the alar layer of deep cervical fascia. This space is commonly referred to as the retropharyngeal / retrovisceral space. This space ends at the level of T2 vertebra. Lying posterior to the alar fascia but anterior to the prevertebral fascia is the danger space known as the prevertebral or Grodinsky space. This space allows wider spread of infections into the mediastinum. This space is commonly involved by rupture of retropharyngeal space abscesses.
Figure showing retropharyngeal space Parotid space: This space lies between the superficial and deep capsules of parotid gland. This is actually formed by splitting of the superficial layer of deep cervical fascia. The superficial capsule is very thick and strong and is closely adherent to the underlying parotid gland. Multiple septa could be seen running from the superficial capsule into the gland forming numerous intraglandular compartments. Infections of parotid gland cannot pierce the tough lateral capsule, instead they present medially with easy access to the lateral pharyngeal space. From the lateral pharyngeal space infections may progress to the retropharyngeal space. This is one of the most feared complication of parotid space infections.
Figure showing parotid space
II. PHYSIOLOGY – Answer any FOUR: (4 x 5 = 20) 1. Physiology of bone conduction. During the middle of 18th century it was found out that sound can traverse through solids. It was during the 19th century it was accepted that humans could hear by bone conduction. Factors contributing to bone conduction hearing include: 1. Sound radiated into the ear canal 2. Middle ear ossicle inertia 3. Inertia of cochlear fluids 4. Alteration of cochlear space 5. Pressure transmission via the CSF fluid Studies have demonstrated that among these factors the inertia of the cochlear fluid is the most important determinant of bone conduction of sound. Human skull vibrates differently with different sound frequencies. At frequencies below 400 Hz the skull moves as a whole with rigid body motion. At higher frequencies 400 - 1 KHz the skull acts as a mass spring system. At frequencies above 1 KHz wave propagation of the skull dominates the skull vibratory response. Role of external auditory canal in bone conduction of sound: When the skull is vibrated by bone conduction stimulation sound is radiated into the ear canal and is subsequently transmitted through vibrations of the ear drum and ossicles to the cochlea. When bone conduction is applied to the mastoid with the ear canal open the sound transmitted via the external auditory canal is 5-20 dB lesser than that of other contributing parts and hence not considered important. When the stimulus is placed over the forehead then the external auditory canal contributes more at frequencies below 1 KHz. When the ear canal is closed then the bone conducted sound is enhanced at low frequencies. This is known as the occlusion effect. Middle ear ossicle inertia: The middle ear ossicular system is suspended by several ligaments, the ear drum and two muscle tendons. Thus it becomes a mechanical mass-spring system which vibrates differently from the surrounding bones in response to bone conduction due to the inertial effect of the mass of the ossicles. This difference in vibration stimulates the cochlea causing the sound to be perceived.
Inertia of the cochlear fluids: Similar to middle ear ossicles, inertial effects cause a relative motion between the cochlear fluids and the cochlear promontory bone. The oval window, round window membranes, and vestibular aqueduct keep this inertia going thus stimulating the end organs of cochlea. Alteration of cochlear space: This was one of the first theories proposed to explain the ability to hear bone conducted sounds. Since cochlear fluids are supposed to be incompressible any reduction in the cochlear space will cause movement of cochlear fluids leading to stimulation of basilar membrane. This helps in perception of sound. This alteration of cochlear space could play a role in bone conduction of high frequency sounds. Pressure transmission from CSF: Variations in CSF pressure caused by the vibrating skull have been assumed to stimulate the basilar membrane via the vestibular aqueduct. This has been one of the recently identified mechanisms of sound transmission by bone conduction.
Figure showing the frequency ranges of human skull vibration modes
2. Physiology of nasal respiration. Nasal respiration plays a vital role in making the inhaled air fit to enter the lungs. This is possible due to: Filtering function: The nasal mucosa efficiently protects the lower air way from particulate matter. This is possible due to deposition of particulate matter in various zones of the nasal cavity. This deposition of particulate matter is dependent on the particle size, shape, weight and aerodynamic properties. Studies have demonstrated that about 60% of particles of size 1 µm diameter are deposited in the nasal cavity. Two most common deposition sites have been identified within the nasal cavity i.e. mucosa posterior to the nasal valve and the anterior aspect of the middle turbinate. Endonasal distribution has been correlated with these two areas because majority of particulate matter gets deposited here. Protective function: This is supposed to be one of the most important functions of nasal airway. It protects the lower airway from the deleterious effects of not only particulate matter and pollutants but also from pathogens like bacteria and viruses. Protection rendered by nasal mucosa is primarily non-specific in nature. This is due to the presence of non-specific protective factors and viable mucociliary clearance mechanism. The following are the commonly present non-specific protective factors present in the nasal secretions: Table showing non-specific protective factors present in nasal secretions. Substance (group) Interferon Proteases Protease inhibitors Lysozyme Antioxidants Example Cathepsin, Elastase, Chymase, Tryptase α 1 protease inhibitor, C1 inactivator Catalases, Gluthathione, Ascorbic acid
Mucociliary clearance mechanism: Inspired air passing through the nasal cavity usually contains particulate matter that is trapped inside the nasal cavity. These particulate matters get
entrapped in the mucociliary mechanism which drives them out of the nasal cavity thereby protecting the lower airway. The mucociliary system is composed of cilia and a mucous blanket that is composed of two layers i.e. superficial viscid gel layer and deeper less viscid sol layer. The ciliary movements occur in the sol layer thereby propelling the viscid gel layer along with particulate matter outside the nasal cavity. Humidifying function: The inspired air is humidified as it passes through the nasal cavity. This mechanism prevents the inspired air from causing drying of the lower airway mucosa. Measurements have shown that the surface area of nasal mucosa is just 120 cm2 . This mucosa will have to humidify about 14,000 litres of inspired air that passes through the nasal cavity per day. The air is not only humidified but is also warmed. Warming of inspired air occurs due to the process of conduction, convection and radiation. During expiration considerable amounts of heat and moisture is removed from the expired air to conserve energy. Air flow resistance & regulation: The nose acts as a dynamic resistor to the inspired air. This nasal resistance helps in preventing alveolar airway collapse by retaining the residual volume. The speed of inspired air at the entrance of nasal cavity is about 2-3 m/sec. This increases to 12-18m/sec at the level of the internal nasal valve. Airflow in the region of internal nasal valve takes an upward angulation of about 60 degrees; hence this area is termed as upstream resistor. Beyond this level the speed of inspired air reduces to 2-3m/s and the direction becomes more horizontal and the flow is directed posteriorly through the choana. Studies have demonstrated that more air passes through the middle meatus than the inferior meatus during normal inspiration. Due to this drastic reduction of air flow speeds beyond the nasal valve area turbulence is caused. This turbulence helps in better heat exchange and humidification of the inspired air. Immune functions of the nasal mucosa: These mechanisms help in protecting the nose from irritants, microbes and allergens. IgA is an immunoglobulin that is characteristic of nasal mucosal defence mechanism. These immunoglobulins are absorbed by the goblet cells present in the lamina propria of nasal mucosa and re-released in combination with a secretory component. Nasal mucosa is also endowed with cellular immune mechanism. These include mast cells, neutrophils, basophils and eosinophils.
Olfaction: This is another function of the nasal airway mechanism. Odoriferous molecules present in the inspired air stimulate the olfactory mucosa present in the roof of the nasal cavity thus playing a role in olfaction. 3. Physiology of Waldeyer’s ring. A ring of lymphoid tissue surrounds the naso pharynx and oro pharynx. These lymphoid tissues are collectively known as the Waldayer’s ring. Waldayer's ring has two components, namely the inner and outer rings. The cervical lymph nodes constitute the outer ring, while the inner ring is constituted by 1. adenoid at the roof of nasopharynx, 2. tubal tonsils or tonsil of Gerlac which surround the pharyngeal ends of eustachean tube. These lymphoid tissues surround the naso pharynx. The lymphoid tissues surrounding the oropharynx also constituting the components of the inner Waldayer’s ring are 1. Lingual tonsil in the posterior 1/3 of the tongue, 2. Palatine tonsils on either side of oro pharynx, and 3. sub epithelial lymphoid tissue found in the posterior pharyngeal wall. All these structures of the inner Waldayer's ring are interlinked. Functions of Waldayer’s rings: These Waldayer's rings constitute an antigen sampling center where the extraneous antigens are caught and sampled stimulating the immune mechanism. Antigens from inspired air are trapped by the adenoid and the tubal tonsils. These antigens in turn stimulate release of immunoglobulin by the B lymphocytes. To facilitate exposure and trapping of antigens the mucosa covering the adenoid is thrown in to grooves called as furrows. These furrows serve to increase the surface area of the adenoid tissue; similarly antigens from ingested food are captured and sampled by the lingual and palatine tonsils. The mucosa covering the palatine tonsils are thrown in to numerous crypts about 18 - 20 in each tonsil. These crypts serve to increase the surface area of mucosa covering the tonsil
4. Physiology of speech articulation. Speech process involves: 1. Speech centres in the brain 2. Respiratory centre in the brainstem 3. Respiratory system 4. Larynx 5. Pharynx 6. Nose / nasal cavities/sinuses 7. Structures of mouth and facial musculature Speech centres in central nervous system: Centres for speech recognition and production is situated on the left hemisphere in 90% of right handed individuals, 60% of left handed individuals and in 30% of ambidextrous individuals. Speech recognition and linguistic expression are located in the Wernicke’s area of brain; this involves input from visual and auditory areas; from this area stimuli are sent to Broca’s area where vocalization control is located. Coordination of oral motor mechanism is very essential for generating complex speech sounds. This takes place at the level of cerebral motor cortex. Respiration: Respiration before phonation is slightly different from that of normal breathing. Inspiration is somewhat quicker and expiration is slightly slowed. Vocal fold vibrations: These vocal folds open and close allowing air from subglottic area to escape in a phased manner. The rate of vibration of vocal folds produces sound. The frequency of these vibrations is highly individualistic and is known as the fundamental frequency of the individual. The fundamental frequency can be adjusted by contraction of intrinsic muscles of larynx especially the thyroarytenoid which is known as the tuning fork of larynx. Positions assumed by vocal folds play a vital role in phonation. 1. When a sound like (f) is produced the vocal folds are held wide apart. 2. Sometimes during speech the vocal folds are completely closed and
Suddenly open to release air from subglottis due to increasing subglottic pressure levels. The sound thus generated is known as glottal stop. 3. Vibrations of vocal folds – this involves four stages. The first stage is closure / adduction where the vocal folds are brought together by contraction of laryngeal muscles. In the second stage the flow from the lungs still persists against the closed glottis causing an increase in subglottic pressure. This stage is known as compression. During the third stage the compressed air in the subglottic region would force the vocal folds to part and would escape. This is known as stage of release. During the fourth stage air flowing between vocal folds they are brought together due to the elasticity of vocal folds and the phenomenon known as Bernoulli’s effect; Bernoulli’s effect is development of negative pressure between the two vocal folds as air flows at a rapid pace between them. The glottis closes and the subglottic pressure rises again. This cycle keeps repeating during the act of phonation and is known as glottic cycle. The loudness of voice is increased by increased contraction of abdominal muscles which increases the effective subglottic pressure causing an increase in the volume of sound generated. The average rate of glottic cycle in female is about 200 – 300 times / sec. In males the average rate of glottic cycle is about 150 times / sec. The rate of glottic cycle can be varied by individuals showing differences in pitch. Resonance: Resonance of sound produced is due to the presence of air in the nasal cavity, nasopharynx and sinuses. Resonances can be adjusted by changes in the position of tongue, jaws and lips. Articulators: These give life and meaning to the voice generated. The articulators include: 1. Lips 2. Jaw 3. Teeth 4. Different regions of tongue 5. Gum ridge 6. Hard palate 7. Soft palate 8. Glottis Importance of tongue as an articulator: The tongue is the most mobile structure inside the oral cavity. It is effectively composed of three articulators tip, blade and back of the tongue. These areas of tongue by articulating with teeth, gum, hard palate and soft palate generate various consonants. The jaw moves upwards and downwards altering the size of the oral cavity thereby providing the space necessary for tongue movements.
5. Nasal reflex. Nose is endowed with various reflexes. These reflexes are aimed at protecting the lower airway from insults, while there are other reflexes that coordinate with physiological functions of other systems. The following are the various reflexes involving the nose: Naso nasal reflex: This reflex is also known as sneezing. This is purely a protective reflex aiming to protect the lower airways from the deleterious effects of substances mixed with the inspired air. This reflex is mediated by the trigeminal and vagal nerves. This reflex may occur due to a variety of stimuli like inhalation of fumes / noxious substances. This reflex is caused by deep inspiration followed by forced expiration against closed glottis. Nasobronchial reflex: This reflex is also known as nasopulmonary reflex / nasolaryngeal reflex. This is an ipsilateral reflex again mediated by trigeminal and vagal nerves. In this reflex nasal stimulation may cause reduction of breathing even cessation (apnoea). This is caused due to constriction of bronchioles and laryngeal inlet. This reflex is more predominant in elderly. This reflex was demonstrated by increased levels of carbon dioxide in blood following packing of nasal cavities. Hence care should be taken while packing the nasal cavities in elderly. This is more common when Bellocq type nasal packs are used. Corporonasal reflex: This reflex is also known as the classic diving reflex. This reflex is caused when face or upper part of the body comes into contact with cold water. This causes cessation of respiration. This reflex also causes bradycardia and contraction of sub mucosal blood vessels under the nasal mucosa. Nasocardiac reflex: In this reflex strong stimulation of nasal mucosa causes bradycardia and reduction in cardiac output and lowering of blood pressure. Nasovascular reflex: In this reflex stimulation of nasal mucosa causes peripheral vasoconstriction. Genitonasal reflex: Sexual arousal / orgasm causes swelling of nasal mucosa, especially the turbinates.
Gastronasal reflex: Strong gastric stimulation causes increased nasal secretion and congestion of nasal mucosa. III. BIOCHEMISTRY– Answer any THREE: (3 x 5 = 15) 1. Biochemistry of lymph. Lymph resembles interstitial fluid in its composition. Lymph capillaries drain the interstitial spaces carrying with them many nutrients including colloidal fat (chyle). Lymph has crystalloid composition more or less similar to that of plasma. The presence of crystalloids contributes to the osmotic pressure of lymph. The protein composition of lymph is very low and contains mostly albumin since globulin cannot readily diffuse into lymph from plasma and hence doses not contribute to the colloidal osmotic pressure (oncotic pressure) as does plasma. Lymph is the main route for transportation of absorbed long chain fatty acids, partially digested fats and cholesterol from the gut via the thoracic duct. 2. Biochemical changes during stridor and after tracheostomy. Stridor causes chronic hypoxic environment. This environment results in: 1. Cessation of aerobic metabolism 2. Exhaustion of high energy intracellular stores 3. Cellular dysfunction 4. Death (ultimate) Stridor leads to respiratory acidosis due to carbon dioxide retention in the body. Ventilatory failure increases the partial pressure of carbon dioxide. This causes a decrease in the bicarbonate levels of human body leading on to acidosis. In these patients serum bicarbonate levels are pretty low. In acute respiratory acidosis the partial pressure of carbon dioxide is raised above 45 mm Hg. In chronic respiratory acidosis certain degree of renal compensation occurs which compensates for acidosis by increased generation of bicarbonate ions. Hence blood biochemistry in these patients reveals increased amounts of serum bicarbonate levels. After tracheostomy pent up carbon dioxide is washed out of the system. This causes a reversal of acidosis. The partial pressure of carbon dioxide is reduced to normal levels.
3. Biochemical changes of CSF during meningitis. In meningitis pressure of CSF is found to be raised. Glucose levels in CSF are lowered in bacterial meningitis while it is normal in viral meningitis. Glucose levels in CSF should always be evaluated in comparison with blood glucose levels also. Reduction of glucose levels in CSF in bacterial meningitis is due to the fact bacteria which involve the meninges consume glucose. Protein levels in CSF will also be found to be elevated in bacterial meningitis due to the presence of immunoglobulins. Neutrophils will be seen in the CSF of patients with bacterial meningitis and Monocytes predominate in patients with viral meningitis. Studies have shown that free sialic acid levels have been found to be elevated in patients with pyogenic meningitis. CSF lactate levels have been found to be increased in patients from the usual 2.5 mmol/L with bacterial meningitis. 4. Biochemical changes of labyrinthine fluids during labyrinthitis. Perilymph is ultra-filtrate of CSF and its composition more or less mirrors that of CSF. Its sodium concentration is more than that of potassium. Glucose levels of perilymph are found to be reduced in patients with suppurative labyrinthitis. Protein levels are also elevated in these patients due to the increased amounts of immunoglobulins present in the perilymph fluid. Endolymph is the only extracellular fluid whose potassium content mirrors that of intracellular fluids. In fact its electrolyte composition resembles that of sea water adding credence to the view that ocean gave birth to all living things. In patients with labyrinthitis potassium from the endolymph begins to leak because of the failure of active potassium transport mechanism by stria vascularis. This loss of potassium proves to be toxic to the cochlear hair cells. Two types of labyrinthitis are associated with bacterial infections. These include Toxic and suppurative labyrinthitis. Toxic labyrinthitis is caused by penetration of bacterial toxins into the perilymph via the round window membrane which becomes abnormally permeable during middle ear infections. This causes release of immunoglobins into the perilymphatic fluids. These bacterial toxins increase the permeability of the membranes to potassium thereby causing an increase in the levels of potassium within the perilymphatic fluid. It is during this stage that labyrinth is irritated and generates abnormal irritation potentials causing tinnitus / giddiness. Increasing levels of immunoglobins causes elevation in the osmolality of the perilymph resulting in influx of excess fluid into the perilymphatic
compartment. This also causes a corresponding rise in the volume of endolymph predisposing to the formation of hydrops. IV. PHARMACOLOGY– Answer any THREE: (3 x 5 = 15) 1. Antimalignancy drugs used in head and neck cancer. Chemotherapeutic agents have a role to play in the management of recurrent head and neck cancers and in patients with metastatic lesions as a result of head and neck malignancy. Studies have shown that combining chemotherapy with irradiation leads to better tumor control rates in these patients. In treating patients with Grade III & IV head and neck malignancies chemotherapy has two roles: 1. Improving the survival rate of these patients 2. Organ preservation Paclitaxel & Dositaxel: These drugs belong to the most active chemotherapeutic agents which are used in the management of head and neck malignancies. This drug is given as iv infusion once in every three weeks. Five doses are administered. This group of drugs are considered to be the first line chemotherapeutic agent in the management of advanced head and neck malignancy. Cisplatin: This drug has remained as the main stay in the management of head and neck malignancy for a long time. This drug in its active form binds to the DNA of the actively dividing cell thereby preventing its replication. It is usually administered in doses of 60-120 mg/m2 over a period of 3 – 6 hours. The limiting factor of this drug is its nephrotoxic effect. Renal parameters should be monitored on a regular basis while the patient is on this drug. Analogues of this drug like carboplatin have been developed with reduced nephro and neurotoxic effects. 5 - Fluorouracil: This drug is an S phase specific uracil analogue. It shows promising effects when administered in 5 days continuous infusion along with cisplatin. Methotrexate: This drug belongs to the antimetabolite group. It interferes with intracellular folate metabolism by binding to the enzyme dihydrofolate reductase inhibiting DNA synthesis. It is usually used in weekly doses of 40 – 50 mg /m2. It is very useful when used in combination with other chemotherapeutic agents. Studies have shown that high dose methotrexate when used as a single agent doesn’t show consistent response.
Cetuximab: Studies have shown that majority of head and neck cancers over express EGFR. This proves to be a good target for this drug as it blocks the expression of EGFR. It is usually administered as a single drug in doses of: Loading dose: 400 mg /m2. Followed by 250 mg /m2 on a weekly basis. Combination chemotherapy is effective than single drug regimen because of the following reasons: 1. Cells resistant to one agent may be sensitive to the other 2. One agent could potentiate the effects of the other there by reducing the dosage of these toxic drugs 3. Dose related drug toxicity could be minimized if these drugs are used in combination. 4. Organ preservation is possible when combination therapy is used. One of the common regimens used is: Cisplatin followed by 4-5 day continuous infusion of 5-flurouracil. In cases where renal parameters suggest nephrotoxicity then cisplatin can be replaced by carboplatin and the same regimen may be continued.
2. Aminoglycoside drugs. These are a group of antibiotics derived from bacteria belonging to Streptomyces genus. Drugs belonging to this group act by binding to the bacterial ribosome 30 s subunit. Some of the drugs belonging to this group may bind to 50 s subunit of bacteria. By binding to these ribosomal subunits bacterial replication is prevented. This binding also causes error in protein synthesis with premature termination of protein synthesis. Drugs belonging to this group are active against a wide variety of gram positive and negative bacteria. Examples of drugs belonging to this group: Streptomycin Gentamycin Neomycin Tobramycin
Drugs belonging to this group are not reliably absorbed from the gut and hence it should be administered parentally for optimal effect. Toxicity: 1. Drugs belonging to this group are ototoxic 2. Nephrotoxic 3. Neurotoxic in high doses These drugs are used to treat predominantly gram negative infections. Since these drugs are poorly absorbed from the gut they are usually administered as topical agents / intravenous agents.
3. Non-sedative antihistamines. The development of non-sedating antihistamines is a welcome development. The first non-sedating antihistamine was introduced in the 1980’s. Terfenadine was the first drug of this group to be introduced. It was followed by acetamizole. Both these drugs were removed from the market due to their undesirable side effects (prolongation of QT interval causing cardiac arrhythmias). Currently available second generation antihistamines are relatively safer than their predecessors. These drugs are not sedating because they don’t penetrate the blood brain barrier and they don’t impair motor activity. These drugs include: 1. Desloratidine 2. Loratidine 3. Fexofenadine 4. Azelastine Drugs belonging to this group have a half-life of 12 – 14 hours, thus favouring once / twice a day dosage regimen. Desloratidine is about 14 times more potent than its congener loratidine. Fexofenadine has not active metabolities and gets excreted in the stools. It depends on transport proteins for its absorption and elimination from the system. Organic anion transporting protein (OATP) is involved. Administration of fexofenadine with fruit juices / with high salt diet causes a 40% reduction in its absorption. P glycoprotein is involved in elimination of this drug from the system. Desloratidine:
This is the metabolite of loratidine. This is one of the more than 12 active metabolities which are generated from loratidine after hepatic metabolism. Food has no impact on the bioavailability of the drug. Its half-life is 12 hours so that it can be administered in convenient od / bd dose regimen. Azelastine: This is the only topical antihistamine currently available. It is rapidly effective, its action manifesting within 30 minutes of administration of the drug. This drug also reduces nasal congestion and is the only drug useful for non-allergic rhinitis. 4. Local anaesthetics. This group of drugs act by binding reversibly to a specific receptor site within the pore of sodium channels in nerves there by blocking ion movements through this pore. This effective blocks the conducting ability of the nerve tissue. These drugs when applied locally on the nerve tissue in adequate concentrations reversibly blocks the action potential generation responsible for nerve conduction. It thus causes both sensory and motor paralysis in the area of innervation. The first local anaesthetic to the discovered was cocaine. This happened due to a fortunate accident. Chemical features potentiating the effect of the drug include: 1. Hydrophobicity – this increases both the potency and the duration of the anaesthetic agent. The receptor sites of sodium gate receptors are said to be hydrophobic. 2. Smaller sized molecule – smaller the size of the drug molecule better and prolonged is its effect because of better tissue penetration. Lignocaine: This is the most commonly used local anaesthetic agent. It produces faster, more intense and long lasting reversible local anaesthesia. Lignocaine can be used as topical anaesthetic agent, and infiltrative anaesthetic agent. For infiltration anaesthesia it is used in 1% - 2% concentration. For surface anaesthesia it is used in 4% - 10% concentrations. When combined with vasoconstrictor like adrenaline the duration of action of lignocaine is prolonged. Bupivacaine: This is another widely used amide anaesthetic agent. This is a potent anaesthetic agent capable of producing prolonged anaesthesia. Uses of local anaesthetic agents: 1. Topical anaesthesia 2. Infiltration anaesthesia 3. Field block anaesthesia
4. Nerve block anaesthesia 5. Spinal anaesthesia 6. Epidural anaesthesia V. PATHOLOGY – Answer any THREE: (3 x 5 = 15) 1. Pathology of nasal polyp. Nasal polyp is simple oedematous hypertrophy of nasal mucosa. Histologically three types of polypi have been identified. 1. Eosinophilic polyp – This is the most common nasal polyp. It is characterised by oedematous stroma, hypertrophy of goblet cells in the overlying respiratory epithelium. Numerous eosinophils can be found in the stroma. The basement membrane appears to be slightly thickened and hyalinised. 2. Inflammatory polyp – In this type there is lack of stromal oedema and goblet cell hyperplasia. The overlying epithelium frequently shows cuboidal / squamous metaplasia. The inflammatory infiltrate is intense with predominance of lymphocytes over eosinophils. The stroma contains numerous fibroblasts. There is slight hyperplasia of seromucinous glands. 3. Polyp with stromal atypia – This rare type of polyp is characterised by stromal atypia. These stromal cells tend to be stellate with hyperchromatic nucleus which is irregular and plump with vesicular cytoplasm. 2. Cholesteatoma. Cholesteatoma is a lesion formed from keratinizing stratified squamous epithelium. Histologically a combination of keratinous material and stratified squamous epithelium is required to make the diagnosis of cholesteatoma. The presence of squamous epithelium in the middle ear cavity is usually considered to be abnormal. The abundant anucleate dead keratin squames account for the flacky white pearly white appearance of cholesteatoma. Unlike the epidermis of skin this squamous epithelium does not contain adnexal structures or rete ridges. There may be adjacent inflamed granulation tissue. Giant cell reaction tissue could be seen for the keratin material. Immunohistochemistry studies show cytokeratin 16 (a marker for hyper proliferating keratinocytes) and Ki 67 (a marker for proliferative activity) show strong expression in cholesteatomatous tissue. 3. Tubercular mastoiditis. Diagnosis of Tuberculous mastoiditis is often not straight forward and is delayed. The granulation tissue of course appears pale. It is always associated bone necrosis and erosion.
Microscopic examination of the granulation tissue demonstrates giant cells (Langhans giant cells / epithelioid giant cells) and caseation necrosis. These patients usually don’t have pain. Deafness is pronounced. Ear drum shows evidence of multiple perforations involving the pars tensa. Complications are common in these patients because of the ability of tuberculous granulation tissue to erode the bone. 4. Malignant melanoma. Superficial spreading melanoma has an in situ phase characterised by increased number of intraepithelial melanocytes. These melanocytes are large and atypical arranged in a haphazard manner at the dermoepidermal junction. Dermal invasion confers malignant potential to the lesion. Tumerogenicity is characterised by a distinct population of melanoma cells in the proliferative phase. Failure of melanocyte maturation and dispersion as the tumor extends downward into the dermis is characteristic of melanoma. Tumor thickness, as defined by the Breslow depth, is the most important histologic determinant of prognosis and is measured vertically in millimetres from the top of the granular layer (or base of superficial ulceration) to the deepest point of tumor involvement. Increased tumor thickness confers a higher metastatic potential and a poorer prognosis. The melanoma staging system initially developed in 1983 by the AJCC and the International Union Against Cancer (UICC) divided melanoma into 4 stages and incorporated tumor thickness and anatomic level of invasion for stages I and II (localized cutaneous disease), with the later recommendation to follow Breslow depth over Clark level when any discordance arose. Stage III disease involved the regional lymph nodes; stage IV disease included distant skin, subcutaneous, nodal, visceral, skeletal, or CNS metastasis. The biopsy report should generally include the following:
• • • • • • •
Tumor thickness (Breslow depth) Presence of ulceration Anatomic level of invasion (Clark level), no longer necessary per 2010 AJCC staging Presence of mitoses, noted as 0 or 1 or more per millimetre squared Presence of regression (associated with lower rates of sentinel node positivity and improved disease-free survival)37 Lymphatic/vessel (lymphovascular) invasion or vascular involvement Host response (tumor-infiltrating lymphocytes)
Immunohistochemical staining for lineage (S-100, homatropine methylbromide 45 [HMB-45], melan-A/Mart-1) or proliferation markers (proliferating cell
nuclear antigen, Ki67) may be helpful in some cases for histologic differentiation from melanoma simulators. Additionally, evidence of lack of maturation with HMB-45 staining and patchy, rather than diffuse, staining with S-100A6 may be helpful for distinguishing spitzoid melanoma from Spitz nevus. V1. MICROBIOLOGY– Answer any THREE: (3 x 5 = 15) 1. Bacteriology of CSOM. Organism found in CSOM includes: a. Streptococcus pneumonia b. Haemophilus influenza c. Moraxella catarrhalis d. Pseudomonas aeruginosa e. Staph aureus The role of anaerobes, fungi and yeast in the pathogenesis of CSOM is not clear. 2. Fusiform bacillus. This organism has been identified as the cause for Vincent’s angina. According to Vincent this is a gram positive organism which stains rather weakly with grams stain. These organism show variations in their gram staining properties. In patients with trench mouth (Vincent’s angina) fusiform bacillus is found to predominate over spirochetes. 3. Rhinosporidiosis. Rhinosporidium seeberi: was initially believed to be a sporozoan, but it is now considered to be a fungus and has been provisionally placed under the family Olipidiaceae, order chritridiales of phycomyetes by Ashworth. More recent classification puts it under DRIP'S clade. Even after extensive studies there is no consensus on where Rhinosporidium must be placed in the Taxonomic classification. It has not been possible to demonstrate fungal proteins in Rhinosporidium even after performing sensitive tests like Polymerase chain reactions. Life cycle: (Ashworth) Spore is the ultimate infecting unit. It measures about 7 microns, about the size of a red cell. It is also known as a spherule. It has a clear cytoplasm with 15 - 20 vacuoles filled with food matter. It is enclosed in a chitinous membrane. This membrane protects the spore from hostile environment. It is found only in connective tissue spaces and is rarely intracellular.
The spore increases in size, and when it reaches 50 - 60 microns in size granules starts to appear, its nucleus prepares for cell division. Mitosis occurs and 4, 8, 16, 32 and 64 nuclei are formed. By the time 7th division occurs it becomes 100 microns in size. Fully mature sporangia measures 150 - 250 microns. Mature spores are found at the centre and immature spores are found in the periphery. The full cycle is completed within the human body. Life cycle (recent): Since rhinosporidium seeberi has defied all efforts to culture it, any detail regarding its life cycle will have to be taken with a pinch of salt. This life cycle has been postulated by studying the various forms of rhinosporidium seen in infected tissue. Trophozoite / Juvenile sporangium - It is 6 - 100 microns in diameter, unilamellar, stains positive with PAS, it has a single large nucleus, (6micron stage), or multiple nuclei (100 microns stage), lipid granules are present. The Intermediate sporangium is about 100 - 150 microns in diameter. It has a bilamellar wall, outer chitinous and inner cellulose. It contains mucin. There is no organised nucleus, lipid globules are seen. Immature spores are seen within the cytoplasm. There are no mature spores. Mature sporangium - 100 - 400 microns in diameter, with a thin bilamellar cell wall. Inside the cytoplasm immature and mature spores are seen. They are found embedded in a mucoid matrix. Electron dense bodies are seen in the cytoplasm. The bilamellar cell wall has one weak spot known as the operculum. Maturation of spores occurs in both centrifugal and centripetal fashion. This spot does not have chitinous lining, but is lined only by a cellulose wall. The mature spores find their way out through this operculum on rupture. The mature spores on rupture are surrounded by mucoid matrix giving it a comet appearance. It is hence known as the comet of Beattee Mature spores give rise to electron dense bodies which are the ultimate infective unit.
Figure showing the recent life cycle theory 1 - Trophozoite (juvenile sporangium) 2 & 3 - Immature bilamellar sporangia 4a & 4b - intermediate sporangia with centrifugal and centripetal maturation of endospores 5 - Mature sporangium with spores exiting through the operculum 6 - Free endospore with residual mucoid material giving it a comet like appearance (comet of Beattie) 7a - Free electron body (ultimate infective unit) 7b - Free electron dense body surrounded by other electron dense bodies which are nutritive granules
4. Adeno virus. These viruses are medium sized (90-100 nm) non enveloped icosahedral viruses composed of a nucleocapsid and a double stranded linear DNA genome. About 55 serotypes have been described. These viruses are the common cause for upper respiratory infections in children. Adeno virus happens to be the largest among non-enveloped viruses. It is because of their large size it is easy for them to be transported into the cell by the endosome (envelope fusion is not necessary). This viron also has a unique spike associated with each penton base of the capsid. This spike aids in the attachment of the virus to the host cell membrane. Adenoviruses possess linear dsDNA genome that can replicate inside the nucleus of mammalian cell using the host’s replication machinery. For a naked virus this one is highly stable and is capable of surviving harsh conditions. These viruses are primarily spread as droplet infection through cough. It can also be transmitted via faces also. Entry of adenoviruses into the host cell involves two sets of interactions between the virus and the host cell. Entry into the host cell is initiated by the knob domain of the fiber protein binding to the cell receptor. The two currently established receptors are: CD46 for the group B human adenovirus serotypes and the coxsackievirus adenovirus receptor (CAR) for all other serotypes. There are some reports suggesting MHC molecules and sialic acid residues functioning in this capacity as well. This is followed by a secondary interaction, where a specialized motif in the penton base protein interacts with an integrin molecule. It is the co-receptor interaction that stimulates internalization of the adenovirus. This co-receptor molecule is αv integrin. Binding to αv integrin results in endocytosis of the virus particle via clathrin-coated pits. Attachment to αv integrin stimulates cell signalling and thus induces actin polymerization resulting in entry of the virion into the host cell within an endosome. Once the virus has successfully gained entry into the host cell, the endosome acidifies, which alters virus topology by causing capsid components to disassociate. These changes as well as the toxic nature of the pentons results in
the release of the virion into the cytoplasm. With the help of cellular microtubules the virus is transported to the nuclear pore complex whereby the adenovirus particle disassembles. Viral DNA is subsequently released which can enter the nucleus via the nuclear pore. After this the DNA associates with histone molecules. Thus viral gene expression can occur and new virus particles can be generated.
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