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The Tamilnadu Dr MGR Medical University D.L.O.

Basic sciences April 2011question paper with solutions

Dr T Balasubramanian

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DLO Basic sciences April 2011 Answer all questions I Elaborate on: 2x15=30 marks

1. Describe the mechanism and disorders related to the process of swallowing in humans. Introduction: The act of swallowing can be considered as a complex activation of the muscles involved in an orderly sequence as orderly like that of the muscles of a Balle dancer. Swallowing is initiated either by voluntary cortical drive or via sensations via the peripheral nervous system. Once the act of swallowing is initiated it continues in an orderly manner. After the initiation the whole act of swallowing is not under voluntary control. The neural network responsible for this reflexive phase of swallowing is known as the central pattern generator. Components of central pattern generator: Brain stem Tractus solitarius Nucleus ambiguus Reticular formation Deglutition is defined as the act of swallowing which causes the food bolus / liquid to the stomach via the mouth, pharynx, and oesophagus. Normal deglutition involves a complex series of voluntary and involuntary muscular contractions. For better understanding the process of deglutition is divided into three phases: Oral Pharyngeal Oesophageal

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Oral phase: This phase of swallowing is voluntary in nature. This phase is subdivided into oral preparatory phase, and oral propulsive phase. During the oral preparatory phase the bolus is processed in such a way that it is rendered swallowable. This phase involves chewing of the food mixed with saliva making it into a bolus which can be smoothly swallowed. During the oral propulsive phase the muscles of the tongue plays an important role in in propelling the food into the oropharyx. When the bolus reaches the oropharynx the involuntary phase of deglutition begins. Cranial nerves involved during the oral phase of deglutition include: Trigeminal, Facial and Hypoglossal nerves. The cerebellum controls these cranial nerve inputs. Disorders involving oral phase of swallowing: Disorders involving this phase of swallowing is usually due to impaired tongue control. These patients have difficulty in chewing food and initiating swallow. These patients also have difficulty in holding liquids inside the oral cavity. Excess liquid inside the oral cavity starts to drool. When attempt is being made to swallow liquid the oropharyngeal reflexes are not initiated causing aspiration. In patients with paralysis involving the facial nerve the lip closure is not precise and complete causing difficulties in holding the bolus inside the oral cavity. These patients also have food stasis in the lateral sulcus due to poor cheek muscle tone. In paralysis involving the hypoglossal nerve the patient is unable to form bolus inside the mouth. Unless a bolus is formed swallowing act is not possible / becomes difficult. Due to reduction in tongue thrust the bolus cannot be propelled into the oropharynx. Due to incomplete contact between the tongue and palate the bolus cannot be efficiently propelled to the oropharynx. In Parkinson's disease repeated tongue rolling may cause difficulty in propelling the bolus into the oropharynx. Disorders involving oral phase of swallowing may cause a delay in the oral phase of swallowing.

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Pharyngeal phase: This phase involves a rapid sequence of overlapping events. This phase involves propulsion of bolus from the pharynx into the upper oesphagus through the cricopharyngeal sphincter. This phase is totally involuntary and reflexive capable of progressing as soon as it is initiated. Critical events involved in this stage include the laryngeal protective sphinteric mechanism which is vital in preventing aspiration of bolus. These events include: a. The soft palate rises b. The hyoid bone and larynx moves upwards and forwards c. The vocal folds adducts and come close to midline d. The epiglottis folds backwards protecting the airway e. The tongue pushes backwards pushing the bolus towards the cricopharyngeal sphincter f. The pharyngeal wall constricts to facilitate backward movement of bolus g. The cricopharyngeal sphincter relaxes due to forward movement of hyoid bone and larynx facilitating easy passage of bolus into the upper oesophagus. This phase of swallowing lasts for about a second and it involves the motor and sensory components of 9th and 10th cranial nerves. Disorders involving this phase of swallowing could case severe feeding impairments. In normal persons during swallow, small amounts of ingested food could be retained in the vallecula and pyriform sinus. In patients with disorders involving the pharyngeal phase of swallowing large amounts of food material may get retained in the vallecula / pyriform fossa causing aspiration when the patient attempts a clearance swallow. Velopharyngeal closure which occurs during this stage helps in preventing nasal regurgitation of food. Imperfect velopharyngeal closure as it occurs due to palatal paralysis / cleft palate / submucosal cleft palate may cause nasal regurgitation during this phase of swallowing. This scenario could also occur when the posterior pillar of tonsil is injured while performing
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tonsillectomy. Presence of severe cervical osteophytes could cause severe swallowing disability involving this phase. In patients with imapired laryngeal elevation due to paralysis of the elevators could lead to cricopharyngeal muscle spasm leading on to aspiration. Reduced laryngeal closure will cause food spillage into the larynx. Pharyngeal muscle paralysis on both sides will cause coating of the lateral pharyngeal wall thereby hindering the swallowing process. Ultimately this could lead to an increase in the pharyngeal bolus transit time. Esophageal phase: In the esophageal phase of swallowing the bolus after crossing the cricopharyngeal sphincter traverses the oesophagus facilitated by the peristalsis of oesophageal musculature. The lower esophageal sphincter relaxes on initiation of the swallowing process. When the bolus enters the stomach the lower esophageal sphincter closes preventing reflux of gastric contents into the oesophagus. This phase of swallowing is involuntary and reflexive being controlled by the medulla. This phase usually lasts less than 20 seconds. Disorders involving this phase could lead to retention of food inside the oesophagus. This retention could be caused by: 1. Mechanical obstruction due to presence of tumors 2. Motility disorders 3. Lower oesophageal sphincter failure

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2. Describe the anatomy of the tympanic membrane and ossicles of the ear. Describe the role of these structures in the mechanism of hearing.
Tympanic membrane is also known as the ear drum. Anatomically it could be considered to be a part of the external ear since it is attached to the medial terminal end of the bony meatus. Functionally speaking it is part of the tympanic cavity. It is more or less oval in shape (egg shaped). It is 9mm in diameter. Its broad portion lies superiorly. It is pearly white in color, thin and semitransparent. When viewed under illumination a trianglular cone of light (reflected light) is seen extending from the centre forwards and downwards. This reflection, or cone of light is due to the sectional shape of the membrane. The ear drum is set with an obliquity of about 55 degrees to the floor of the external meatus. The centre of the ear drum appears retracted, and is known as the umbo. This umbo lies at the apex of the cone of light. Visible as an ivory colored extension upwards from the umbo is the handle of the malleus. If the posterior portion of the membrane is transparent, then the image of the long process of the incus, and occasionally the stapedial tendon may also be seen.

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Figure showing anatomy of ear drum


The ear drum is composed of 3 layers. The outer layer is formed by stratified squamous epithelium, and is continuous with that of the external auditory canal. Any condition affecting the skin of the external canal will also affect the outer layer of the ear drum. Common conditions like dermatitis involving the skin of the external canal can also involve the outer layer of the ear drum. Embryologically outer layer of the ear drum developed from the ectoderm. Myringitis granulosa a common condition affecting the ear drum affects only the outer layer of the tympanic membrane. The middle and inner layers are not involved in this condition. It is commonly caused by infections arising from the external canal. Constant irritation of the ear drum due to presence of wax may also predispose to this condition. Another condition which involves the outer layer of the ear drum is Bullous myringitis. In this condition blebs may be seen in the outer layer of the ear drum. It is commonly caused by viral infections, or mycoplasma pneumonia. It may also be associated with middle ear effusion. The middle fibrous layer from which the ear drum derives its strength and resilience is derived from the mesoderm. This portion is infact sandwiched between the outer squamous lining derived from the ectoderm and inner mucosal lining of the middle ear cavity derived from the endoderm. The ectodermal and mesodermal components of the ear drum arise from the first branchial cleft, while the endodermal component is derived from the pharyngotympanic recess. The middle fibrous layer has two components: 1. radial and 2 circular fibres. The handle of the malleus lie between the middle fibrous layer and the inner mucosal layer of the ear drum. From the handle of the malleus the radial fibres of the middle fibrous layer radiate towards the circumferance of the ear drum. The circular fibres are more prominent and thickened along the circumference of the ear drum. The condensation of the circular fibres are fixed to the tympanic sulcus at the medial end of the external auditory canal. This middle firbous layer is absent in the attic area of the ear drum. The fibrocartilagenous ring and the fibrous layer of the ear drum are deficient superiorly. This deficient area is known as the notch of Rivinus. The attic portion of the ear drum which lack the middle layer is known as the pars flaccida, while the rest of the drum which has all the three layers is known as pars tensa. The chorda tympani nerve which is a branch of the facial nerve run between the middle fibrous and inner mucosal layers of the ear drum. The skin of the external canal and the outer lining of the tympanic membrane are unique in a sense that they lack frictional and abrasive contacts which is common with the skin lining elsewhere in the body. Desquamated keratin does not accumulate on the surface of the tympanic membrane, or in the deep external meatus, because the skin lining here is endowed with a peculiar Drtbalu's otolaryngology online

feature known as Migration. The surface layers of the skin of the ear drum, and the surface keratin move towards the periphery of the membrane, and then slowly along the external meatus to the exterior. Derangements of this unique feature is associated with some of the diseases of the external ear. The inner layer of the ear drum derived from the endoderm of the pharyngotympanic recess is continuous with that of the mucosal lining of the middle ear cavity. Blood supply: The external surface of the ear drum receives its blood supply from the deep auricular branch of the maxillary artery. This small artery leaves the first part of the maxillary artery behind the neck of the mandible and gains access into the external canal by piercing the anterior wall behind the mandibular joint. It sends small branches into the membrane from the whole circumference of the pars tensa and one or more manubrial branches that descend on the handle of mandible from above. The internal surface of the ear drum is supplied from behind by the stylomastoid branch of the posterior auricular artery, and from the front by the tympanic branch of the maxillary artery. The superficial veins open into the external jugular vein; and those on the internal surface drain into the transverse sinus and veins of the dura mater, and partly into the venous plexus on the eustachean tube.

Nerve supply: The innervation of the posterior half of the ear drum is by the auricular branch of the X nerve and the anterior half is by the auriculotemporal branch of the Vth nerve. The inner surface of the ear drum is supplied by the tympanic branch of the IXth nerve.

The middle ear contains three ossicles which play a very important role in sound transmission. These ossicles are: 1. Malleus 2. Incus 3. Stapes Malleus: This bone is shaped like a hammer hence the name. This is the largest of the three ossicles of the middle ear cavity. It has a head, neck and three processes arising from below the neck. The overall length of the malleus ranges between 7.5 - 9 mm. Its head lies in the attic region of the middle ear effectively dividing the attic into an anterior portion and a posterior one. The anterior portion lie anterior to the handle of the malleus, while the posterior portion lie behind the handle of the malleus. During surgical procedures for attic cholesteatoma clipping of this head will improve the exposure in the attic Drtbalu's otolaryngology online

region. The head of the malleus on its posteriomedial surface has an elongated saddle shaped cartilage covered facet for articulation with the incus. This articular surface is constricted near its middle dividing the articular facet into a larger superior and a smaller inferior portions. The inferior portion of the articular facet lies at right angles to that of the superior portion. This projecting lower portion is also known as the cog or spur of the malleus. Below the neck the bone broadens and gives rise to the following: the anterior process from which a slender anterior ligament arises to insert into the petrotympanic fissure; the lateral process which receives the anterior and posterior malleolar folds from the annulus tympanicum, and the handle which runs downwards, medially and slightly backwards between the mucous and fibrous layers of the tympanic membrane. On the deep medial surface of the handle there is a small projection into which the tendone of the tensor tympani muscle inserts. Additionally the malleus is supported by the superior ligament which runs from the head to the tegmen tympani.

Figure showing the malleus Incus: This bone is shaped like an anvil. It articulates with the malleus and has a body and two processes. The body lies in the attic and has a cartilage Drtbalu's otolaryngology online

covered articular facet corresponding to that of the malleus. The short process projects backwards from the body to lie in the fossa incudis. It is infact attached to the fossa incudis by a short ligament. The long process of the incus descends into the mesotympanum behind and medial to the handle of the malleus. At its tip there is a small medially directed lenticular process which articulates with the stapes. The long process of the incus has precarious blood suppy. This portion of the incus is prone for undergoing necrosis in disease conditions.

Figure showing the incus The stapes: The stapes consists of a head, neck, two crura and a base (footplate). The head of the stapes points laterally and has a small cartilage covered depression for articulation with the lenticular process of the incus. The tendon of the stapedius muscle attaches to the posterior part of the neck and the upper part of the posterior crura. The neck of the stapes gives rise to two crura, the anterior crura is thinner and less curved than the posterior crura. The two crura join the foot plate which closes the oval window during life. The average dimensions of the foot plate is 3mm x 1.4mm. The long axis of the foot plate is almost horizontal, with the posterior end being slightly lower than Drtbalu's otolaryngology online

the anterior.

Figure showing the stapes Role played by the ear drum and ossicles in hearing: Sound which impinges on the ear drum sets it into vibrations. These vibrations are transmitted by the middle ear ossicles to reach the round window membrane which conduct it to the inner ear fluids. Initially the vibrations of the ear drum belong to the low pressure high displacement variety. These vibrations are not capable of vibrating the inner ear fluids. For vibrating the inner ear fluids the stimulus should be of low displacement high pressure variety. This change in the type of vibration is brought about by the impedance matching mechanism of the middle ear cavity. Two processes are involved in the impedance matching mechanism of middle Drtbalu's otolaryngology online

ear. They are: 1. The area of the tympanic membrane is larger than that of the stapes foot plate in the cochlea. The forces collected over the ear drum are concentrated over a smaller area, thus increasing the pressure over oval window. The pressure is increased by the ratio of these two areas i.e. 18.75 times. 2. The second process is the lever action of the middle ear bones. The arm of the incus is shorter than that of the malleus, and this produces a lever action that increases the force and decreases the velocity at the stapes. Since the malleus is 2.1 times longer than the incus, the lever action multiplies the force by 2.1 times. Buckling effect of ear drum: The ear drum curves from its rim to its attachment to the manubrium. The buckling effect causes greater displacement of the curved ear drum and less displacement for the handle of the malleus. This causes high pressure low displacement system. Role of ear drum in sound conduction: The ear drum conducts sound from the external ear to the middle ear. Bekesy postulated that the ear drum moved like a stiff plate up to frequencies of 2 kHz. He also suggested that the inferior edge of the drum is flaccid and moves the most. At frequencies above 6 kHz the vibrating pattern becomes more complex and chaotic. This reduces the efficiency of sound transfer mechanism. The handle of the malleus is attached to the centre of the ear drum. This allows sound vibrations on any portion of the ear drum to be transmitted to the ossicles.

II Write short notes on:

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1. Mastoid air cell system: Is considered to be an important contributor to the physiology of middle ear function. According to Tumarkin the mastoid air cell system served as an reservoir of air and serves as buffer system to replace air in the middle ear cavity temporarily in case of eustachean tube dysfunction. The mean volume of air in the mastoid air cell system could be about 5-8 ml. CT scan evaluation of temporal bone is considered to be the best modality to assess mastoid air cell system.
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The penumatization of mastoid air cell system can be divided into 3 types: Sclerotic mastoid Pneumatization is absent Diploic mastoid Pneumatization partial Pneumatic mastoid Full and complete pneumatization The mastoid air cell system is covered with highly vascular cuboidal epithelium. The contact between the blood vessels and the basement membrane is rather close resembling that of alveoli where extensive gaseous exchange takes place. The mastoid air cell system is categorized according to various regions of temporal bone. These include: a. Squamo mastoid This area include air cells around antrum, central mastoid tract and peripheral air cell tract. b. Perilabyrinthine cells These can be divided into supra labyrinthine and infralabyrinthine air cells c. Petrosal air cells Petrosal air cells and petrous apex air cells d. Accessory air cells These cells include zygomatic air cells, occipital air cells, squamous air cells and styloid air cells. Patients with poor pneumatization of mastoid air cell system are more prone to develop adhesive otitis media following middle ear infections as the normal buffering system of the mastoid pneumatization is not adequate in them. Treatment of secretory otitis media with effusion is more effective in a patient with well developed mastoid air cell system when compared to that of patients with sclerosed ones. 2. Left recurrent laryngeal nerve The course taken by the vagus nerve differs between the right and the left sides. The left vagus nerve follows the carotid artery into the mediastinum crossing anterior to the aortic arch. The left recurrent laryngeal nerve arising from the vagal nerve just below the aortic arch loops medially under the aorta and ascends within the tracheoesophageal groove. The anterior bronchoesophageal artery supplies the left vagus nerve. The approximate length of the left recurrent laryangeal nerve is 12 cms. Considering the extra length and the distance the left recurrent laryngeal nerve has to travel, it is the common nerve affected by diseases / disorders / trauma etc. e
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u ntil it approaches

Diagram showing left recurrent laryngeal nerve The recurrent laryngeal nerve has significant but varying relationship with
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the inferior thryoid artery. On the left side, the recurrent laryngeal nerve passes behind the inferior thyroid artery in 50% of the cases and anterior to the artery in 20% of cases and may lie in between the branches of the inferior thyroid artery in 30% of cases. The left recurrent laryngeal nerve is more susceptible to injuries than the right because of its longer and more extensive course. It also lies superficial in the left tracheoesophageal groove.

3. Nasal cycle This is defined as rhythmic alternating side to side fluctuation of nasal airflow. This fluctuation is caused by alternating congestion and decongestion of nasal mucous membrane and changes in the size of nasal turbinates. Kayser first coined the term nasal cycle even though it was known to yogis for a long time. These cyclic changes occur between 4-12 hours and are constant for each individual. Even though nasal cycle is demonstrable in nearly 80% of adults it is more difficult to see in children. The cyclical changes seen in nasal cycle are produced by vascular activity, particularly by the amount of blood present in venous sinusoids (capacitance vessels). These changes are dependent on discharge of autonomic nervous system. Nasal secretions are also cyclical. Secretions are found to be increased on the side with the greatest airflow. Factors that modify nasal cycle: 1. Allergy 2. Infection
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3. Exercise 4. 1. Hormones 2. 3. Pregnancy 4. Fear / emotions 5. Sexual activity 6. High levels of CO2 in the inspired air causes a reduction in the nasal resistance 7. Drugs that block the action of noradrenaline cause reduction in the nasal cycle. The reason for nasal cycle still remains to be studied.

4. Bacteriology of CSOM CSOM can be differentiated from ASOM bacteriologically. In chronic suppurative otitis media bacteria enters the middle ear cavity from the nasopharynx via the eustachean tube, and from the external auditory canal via the perforation into the middle ear cavity. Bacteria present in the ears of CSOM patients may be aerobic / anaerobic. Aerobic organism include Pseudomonas aeruginosa, E coli, Staphylococcus aureus, staphylococcus pyogenes proteus and klebsiella. Anaerobic organism include Bacteroids, peptostreptococcus and propionobacterium. Among these bacterial organisms enumerated pseudomonas aeruginosa has been blamed for deep seated and progressive destruction of the middle ear cavity and mastoid structures through its toxins and enzymes. Fungi have also been increasingly isolated from aural discharge in patients with CSOM. Isolated fungi include candida albicans, and aspergillus fumigatus. Currently bacterial biofilms have been postulated to play a role in middle ear infections in patients with CSOM. Presence of biofilms provides a protective environment for bacteria to multiply in the middle ear cavity. Biofilm also enables the microbes to develop resistance to the commonly
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used antibiotics. 5. Vidian nerve: The vidian nerve is formed by post synaptic parasympathetic fibers and presynaptic sympathetic fibers. This is also known as the Nerve of pterygoid canal. Nerves that gets involved in the formation of vidian nerve: 1. Greater petrosal nerve (preganglionic parasympathetic fibers) 2. Deep petrosal nerve (post ganglionic sympathetic fibers) 3. Ascending sphenoidal branch from otic ganglion Vidian nerve is formed at the junction of greater petrosal and deep petrosal nerves. This area is located in the cartilagenous substance which fills the foramen lacerum. From this area it passes forward through the pterygoid canal accompanied by artery of pterygoid canal. It is here the ascending branch from the otic ganglion joins this nerve. The vidian nerve exits its bony canal in the pterygopalatine fossa where it joins the pterygopalatine ganglion. Vidian canal: It is through this canal the vidian nerve passes. This is a short bony tunnel seen close to the floor of sphenoid sinus. This canal transmits the vidian nerve and vidian vessels from the foramen lacerum to the pterygopalatine fossa. According to CT scan findings the vidian canal is classified into: Type I: The vidian canal lies completely within the floor of sphenoid sinus Type II: In this type the vidian canal partially protrudes into the floor of sphenoid sinus Type III: Here the vidian canal is competely embedded in the body of sphenoid bone Vidian neurectomy is considered as a treatment in patients with:

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1. Chronic epiphora (crocodile tears) 2. Vasomotor rhinitis not responding to medical management 3. In the management of intrinsic rhinitis 6. Prussak's space: This space is named after the Russian otologist Alexander Prussak. This is a small middle ear recess which lies medial to the pars flaccida. Boundaries: Superiorly: Scutum and lateral malleolar ligament Lateral: Pars flaccida Inferior: Lateral process of malleus Medial: Neck of the malleus It communicates with the posterior pouch of Troeltsch. Clinical significance: Cholesteatoma invariably starts in this space. It begins as a retraction pocket involving pars flaccida. Cholesteatoma from this space spreads via: Posterior epitympanum through the superior incudal space to involve the mastoid antrum. Posterior mesotympanum: Inferiorly via the pouch of Von Troeltsch to involve stapes, round window, sinus tympani and facial recess. Anterior epitympanum: Anterior to head of malleus it can gain access to supratubal recess via the anterior pouch of Von Troeltsch. 7. Developmental anamolies of the nose: Developmental anamolies of nose and paranasal sinuses are rare manifestations involving development of aerodigestive tract. Children afflicted with these abnormalities may manifest with life threatening airway obstruction and feeding difficulties. Classification of developmental abnormalities of nose and sinuses: 1. Errors at the anterior neuropore 2. Errors of central midface 3. Errors of bucconasal membrane Developmental errors involving anterior neuropore:
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a. Glioma Isolated heterotrophic glial tissue b. Menigocele / encephalocele Patent central nervous system communication Encephaloceles can occur in a paramedian position as nasoethmoidal encephalocele. Encephaloceles can occur laterally through a defect in the medial orbital wall causing a naso orbital encephalocele. Basal encephaloceles herniate posterior to cribriform plate. Histopathologically all encephaloceles have the following components: Glial component Astrocytes surrounded by collagen Submucous glands Calcification Nasal septal cartilage Presence of ependymal tissue is consistent with that of encephalocele. Its presence helps in differentiation between encephalocele and gliomas. Intranasal gliomas: Usually presents as pale polypoidal masses protruding from the nasal cavity. They arise from the lateral nasal wall close to the middle turbinate. Rarely they could also arise from nasal septum. Nasal dermoid: These are frontonasal inclusion cysts /tracts caused by embryological errors localized to the anterior neuropore. Congenital dermoids contain ectodermal and mesodermal elements, this is in contrast to teratoma which contains components of all three germ layers. Arhinia: This is congenital absence of nose which could be due to: a. Abnormal migration of neural crest cells b. Failure of fusion between medial and lateral nasal processes c. Overgrowth and premature fusion of medial nasal processes d. Lack of resorption of nasal epithelial plugs Polyrihinia: This malformation is characterised by multiple nose like tags in the
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midface region. This usually results from incomplete development of frontonasal process. This anamoly causes separation of developing lateral portions of the nose. Proboscis lateralis: This is caused by mesodermal proliferation disorders. These disorders usually occur close to the nasal pit area. Since there is no mesoderm in this area support for epidermis is lost. Nasolacrimal duct are also not formed in these patients. The resultant structure resembles trunk of an elephant. Nasolacrimal duct cysts: These uncommon abnormalities involve the inferior meatus. Usually the nasolacrimal duct canalization begins in the lacrimal end and proceeds in an inferior direction. Failure of canalization process leads to this deformity. Developmental errors involving the bucco nasal membrane: This causes choanal atresia. Choanal atresia could be bony / membranous. Unilateral or bilateral. Bilateral choanal atresia is an emergency as infants are obligate nasal breathers. Choanal atresia are usually caused by: 1. Persistence of buccopharyngeal membrane 2. Persistence of nasobuccal membrane 3. Abnormal persistence of mesoderm in the choanal region 8. Intrinsic muscles of larynx: These muscles move the vocal folds and thus play a vital role in the process of phonation. Posterior cricoarytenoid muscle: These are small paired muscles extending from the posterior portion of cricoid cartilage to the muscular process of arytenoid cartilage. Contraction of these muscles rotates the
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arytenoid cartilages medially abducting the vocal folds. These muscles are supplied by the recurrent laryngeal nerve. This is the only muscle that opens the larynx.

Diagram showing Posterior cricoarytenoid muscle in action

Adductors of vocal folds: Lateral cricoarytenoid muscle: This muscle arises from the superior border of the lateral part of cricoid cartilage. It is inserted into the front of the muscular process of arytenoid. It adducts the vocal ligaments by rotating the arytenoids medially.

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Interarytenoid muscles: comprise paired oblique arytenoid muscles and unpaired transverse arytenoid muscle. They adduct the vocal folds. Thyroarytenoid muscle: This muscle is responsible for the tension of vocal folds thereby determining its pitch of vibration. This thin muscle lies parallel with and lateral to the vocal folds. It supports the ventricular wall and its appendix. It arises from the lower half of the angle of thyroid cartilage and from the middle cricothyroid ligament. Its fibers pass backwards and laterally to be inserted into the base and anterior surface of arytenoid cartilage. Thyroarytenoid muscle essentially is composed of three parts: Thyrovocalis:originates from the inner surface of the thyroid cartilage, just below the thyroid notch and inserts on the vocal process of the arytenoid cartilage. When this muscle contracts it opens the crico-thyroid visor. It can also tense the vocal folds when it acts in tandem as an antagonist with the cricothryroid muscle. This muscle is also known commonly as the vocalis or the medial part of the thyroarytenoid muscle.
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Thyromuscularis: this part of the thyroarytenoid, known as the lateral section, inserts higher on the arytenoid cartilage on to the muscular process. It has the same function as the lateral cricoarytenoid the vocal folds with adduct and lengthen along the free edge. This muscle may also be called the muscularis or the lateral part of the thyroarytenoid muscle. Thyroepiglottis: also known as the superior thyroarytenoid muscle. Some anatomists say this muscle is not present in all individuals. It originates higher on the internal surface of the thyroid cartilage and has a more oblique direction back down toward the muscular process of the arytenoid where it inserts. When present this muscle seems to serve as a relaxer of the vocal fold. It may also possibly be responsible for changing and controlling the internal dimensions of the epilarynx and false vocal folds.

9. Osteomeatal complex: Ostiomeatal complex: This term is used by the surgeon to indicate the area bounded by the middle turbinate medially, the lamina papyracea laterally, and the basal lamella superiorly and posteriorly. The inferior and anterior borders of the osteomeatal complex are open. The contents of this space are the aggernasi, nasofrontal recess (frontal recess), infundibulum, bulla ethmoidalis and the anterior group of ethmoidal air cells. This is infact a narrow anatomical region consisting of : 1. Multiple bony structures (Middle turbinate, uncinate process, Bulla ethmoidalis) 2. Air spaces (Frontal recess, ethmoidal infundibulum, middle meatus) 3. Ostia of anterior ethmoidal, maxillary and frontal sinuses. In this area, the mucosal surfaces are very close, sometimes even in contact causing secretions to accumulate. The cilia by their sweeping movements pushes the nasal secretions. If the mucosa lining this area
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becomes inflamed and swollen the mucociliary clearance is inhibited, eventually blocking the sinuses. Some authors divide this osteomeatal complex into anterior and posterior. The classic osteomeatal complex described already has been described as the anterior osteomeatal complex, while the space behind the basal lamella containing the posterior ethmoidal cells is referred to as the posterior ethmoidal complex, thus recognising the importance of basal lamella as an anatomical landmark to the posterior ethmoidal system. Hence the anterior and the posterior osteomeatal complex has separate drainage systems. So when the disease is limited to the anterior compartment of the osteomeatal complex, the ethmoid cells can be opened and diseased tissue removed as far as the basal lamella, leaving the basal lamella undisturbed minimising the risk during surgery.

10. Rhinosporidium seeberi: 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.
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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. A 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. Intermediate sporangium - 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
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operculum. Maturation of spores occur 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.

Life cycle of rhinosporidium seeberi 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 apperance (comet of Beattie)
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7a - Free electorn body (ultimate infective unit) 7b - Free elecctron dense body surrounded by other electron dense bodies which are nutritive granules Theories of mode of spread:
1. 2. 3. 4.

Demellow's theory of direct transmission Autoinoculation theory of Karunarathnae (responsible for satellite lesions) Haematogenous spread - to distant sites Lymphatic spread - causing lymphadenitis (rarity)

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