Tamil Nadu Dr MGR Medical University ENT MBBS Prefinal Feb 2009 question paper with solution

8/8/2019 Tamil Nadu Dr MGR Medical University ENT MBBS Prefinal Feb 2009 question paper with solution

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MBBS (Prefinal Otolaryngology February 2009)

Essay questions: 2x15=30 marks

1. Describe the etiopathology of conductive deafness. Describe the types oftympanoplasty


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Definition:

Conductive deafness is defined as deafness caused due to defect in the sound

conducting mechanism of the ear. A majority of these conditions can be correcte

surgical procedures.

Causes of conductive deafness can be classified into:

a. External ear causes

b. Causes involving the ear drum

c. Middle ear causes

d. Inner ear causes

External ear causes:

These are the common causes of conductive deafness. These conditions preven

sound waves from reaching and vibrating the ear drum. They include:

Impacted cerumen

Osteomas of external auditory canal

Atresia of external auditory canal

Impacted foreign bodies in the external ear (rare)

Tumors of external canal

Causes involving the ear drum:

Tympanic membrane plays a vital role in sound connection mechanism. Failure

ear drum to vibrate adequately will cause conductive deafness. Common such c

include:

Perforations involving the ear drum Could be due to CSOM / ASOM / Trauma.

Deafness is directly proportional to the size of the perforation. Sometimes if the edrum perforation occurs close to the round window niche then deafness will be m

pronounced. This condition can be surgically managed by closing the perforation

suitable graft material (Myringoplasty).

Tympanosclerotic plaques on the ear drum These plaques are calcareous depo

over the mucosal layer of the ear drum. The presence of these patches / plaques

prevent the normal vibration of the ear drum predisposing to conductive deafness


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Causes involving the middle ear:

Any condition that prevents the normal vibration of the middle ear ossicles and th

medial surface of ear drum will lead to conductive deafness. These include:

Fluid accumulation in the middle ear cavity Seen in secretory otitis media, acute

decompression sicknessHematoma in the middle ear cavity Collection of blood inside middle ear cavity

to trauma) dampens the vibrations of the middle ear ossicles.

Disruption of ossicular chain Discontinuity of ossicular chain will cause severe

degree of conductive deafness. Disruptions can be caused by trauma, erosion o

ossicles due to cholesteatomatous matrix.

Congenital fixation of ossicular chain One of the rare causes of congenital

conductive deafness. These patients improve with ossiculoplasty procedures.

Fixation of foot plate of stapes Occurs in otosclerosis. This causes difficulties i

transmission of sound to inner ear.

Ventilation problems of middle ear cavity Loss of normal middle ear air volume

cause dampening of the vibrations of the ear drum and ossicles. This is common

caused by eustachean tube malfunction.

Tumors of middle ear cavity May prevent normal vibration of ossicular chain ca

conductive deafness.


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2. Discuss the etiopathology of malignant tumors of maxilla. Add a note on its

investigations and surgical management

Causes of malignant tumors of maxilla include:

a. Exposure to hard wood dust (African Mahogany) Adenocarcinoma

b. Soft wood dust Squamous cell carcinoma

c. Nickel refining (chromium workers) Cause squamous cell carcinoma

d. Leather and textile workers

e. Exposure to Isopropyl alcohol & volatile hydrocarbons

f. Snuff

e. Human papilloma virus exposure

About a quarter of malignant lesions of nose and paranasal sinuses originate from

maxillary antrum.Commonest malignant lesion involving the maxillary sinus is squamous cell

carcinoma. Other possible malignant lesions include: Basal cell carcinoma,

esthesioneuroblastoma, plasmocytoma, lymphoreticular tumors, malignant tumor

involving minor salivary glands, adenocarcinoma, undifferentiated carcinomas,

sarcomas, inverted papilloma turning malignant and malignant neurogenic tumor

Harrison classified malignant tumors of the maxillary sinus into four stages. This

staging process facilitated assessment of prognosis and deciding the optimal

treatment modality.T1- Tumor limited to antral mucosa without evidence of bone erosion

T2- Tumor inside the antrum with evidence of bone erosion. The facial skin, orbi

ethmoids and pterygopalatine fossa are not involved.

T3- Involvement of orbit, ethmoids, facial skin

T4- Tumor extension to nasopharynx, sphenoid sinus, cribriform plate or

pterygopalatine fossa


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Recent classification of maxillary antral malignancy is TNM classification.

T- indicates primary tumor

N- Nodal status

M- distant metastasis

T1 Tumor limited to antral mucosa with no evidence of bone destructionT2 Tumor with evidence of bone destruction. In this stage the posterior wall of

maxilla is spared. There may also be extension through the hard palate and mid

meatus

T3 In this stage tumor involves the posterior wall of maxilla, subcutaneous tissu

skin over the cheek and orbital floor

T4 Tumor involving the orbit / cribriform plate / Skull base / Nasopharynx / Sphe

sinus / Frontal sinus

N Nodal status

N1 Metastasis in a single ipsilateral lymph node measuring 3 cms or less in its

greatest dimension

N2 Metastasis in a single ipsilateral node measuring 3cms 6 cms in its greate

dimension / multiple ipsilateral nodes not exceeding 6cms in their greatest dimen

bilateral or contralateral nodes not exceeding 6cms in their greatest dimension.

Substages of N2:

N2a Single ipsilateral node which is more than 3 cms but less than 6 cms in its

greatest dimensionN2b Metastasis to multiple ipsilateral nodes which measure more than 3 cms b

less than 6 cms in their greatest dimension

N2c Metastasis to bilateral / contralateral nodes with none of them measuring m

than 6 cms in their largest dimension

N3 Metastasis to regional nodes measuring more than 6 cms in their greatest

dimension

Tumor spread:

Antral tumors spread in to:1. Nasal cavity

2. Ethmoid

3. Orbit via the infra orbital fissure

4. Soft tissues over the cheek by eroding the anterior wall

5. Palate / alveolar ridge by dental foramina

6. Buccal sulcus

7. Infratemporal fossa by erosion of posterior wall of antrum

Management:Of malignant tumors of maxillary antrum is dependent on tissue diagnosis and ex


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of the lesion. Tissue biopsy is a must. All these patients should under go tissue

biopsy procedures like endoscopic antrostomy / caldwell luc surgery to obtain tiss

sample for histopathological diagnosis.

Role of imaging:

Imaging plays a vital role in the assessment of anatomical site of the lesion,

extensions if any can also be clearly seen. CT scanning and MRI scanning perfo

before surgery assists in staging of the disease and in planning the optimal surgic

treatment modality.CT scans are highly accurate in identifying bony erosion / remodelling. Bony

remodelling is commonly seen in malignant tumors involving salivary glands, larg

lymphoma and melanoma. It is also very accurate in accessing orbital involveme

it shows clear delineation of the lamina papyracea. It is more accurate than MRI

scanning in identifying orbital invasion / invasion of anterior skull base.

MRI scans are pretty useful in the study of perineural invasion of tumors like

adenocystic carcinoma.

Surgical management:

The following are the various surgical modalities:

1. Total maxillectomy

2. Medial maxillectomy3. Lateral rhinotomy (limited malignancies)

4. Anterior craniofacial resection

5. Anterior midfacial degloving

Irradiation:

Patients with stage I antral malignancies can be subjected to full curative dose of

radiotherapy. Pre operative / post operative radiation can be followed according

prevailing portocol of the institution.Sandwich therapy:

In this type of therapy these patients receive half the dose of curative radiotherap

surgery is performed after 6 weeks. Six weeks following surgery these patients

receive the remaining half of the curative dose of radiotherapy. The advantage o

treatment modality is the tumor gets down staged following radiotherapy making

process of surgery that much easier. Post operative radiotherapy helps in the

completion of treatment. Nodal metastasis if any (occult) will be sterilized by pos

irradiation in these patients.


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3. Write short notes on: 6x5=30 marks

a. Nasal polyposis

Nasal polyp:Polyp is a Latin word meaning polypous (many footed).

Definition:Polyp is defined as simple oedematous hypertrophied mucosa of the nasal cavity

can be unilateral / bilateral.

Causes of nasal polyp:

1. Infections

2. Allergy

3. Polyp due to mucovisidosis

Classification:

Nasal polyp can be classified as:

1. Simple polyp

. Ethmoidal polypi

. Antrochoanal polyp

2. Fungal polyp

3. Malignant polyp

Differences between antrochoanal polyp and ethmoidal polypi

Ethmoidal polypi Antrochoanal polyp

Seen in adults Seen in children and adolescents

Allergy is the common cause Infection is the common cause

Multiple (bunch of grapes) Unilateral

Arises from ethmoidal labyrinth Arises from maxillary antrum

Seen easily on anterior rhinoscopy Seen commonly in post nasal exam

X ray PNS may show hazy ethmoids and

normal maxillary sinuses

X ray PNS shows hazy maxillary antrum

Mostly bilateral Usually unilateralRecurrence is common Recurrence is uncommon

Polypectomy Caldwel luc surgery in recurrent cases

Nasal polyp is a surgical condition. All these polypi should be removed from the

cavity. It is usually performed under direct vision using a nasal endoscope. After

removal these patients should be ideally placed under topical steroids. Steroids

only helps in reducing the inflammation but also shrinks the polypoidal mucosa.

polypoidal material removed during the surgical procedure should be sent for


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histopathological examination to rule out the presence of malignant tissue. It is n

uncommon for a patient with malignant mass in the nasal cavity to present with a

sentinel polyp anterior to the malignant nasal mass.

Nasal polyp should be differentiated from that of a hypertrophied turbinate. The

following points help in the process of differentiation.

Polyp Turbinate

Insensitive to touch Sensitive to touch

Can be probed all around Cannot be probed all around

Pale and glistening Looks fleshy and red

Soft to touch Firm to touch

Shrinks very little with nasaldecongestants Shrinks significantly with nasaldecongestants

b. Rhinosporidiosis:

Definition: It has been defined as chronic granulomatous disease characterized b

production of polypi and other manifestations of hyperplastic nasal mucosa. Theetiological agent happens to be 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. More recent classifi

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 b

possible to demonstrate fungal proteins in Rhinosporidium even after performing

sensitive tests like Polymerase chain reactions.

Incidence and Geographical distribution:

Of all the reported cases 95 % were from India and Srilanka. An all India surveyconducted in 1957 revealed that this disease is unknown in states of Jummu &Kashmir, Himachal pradesh, Punjab, Haryana, and North Eastern states of India. state of TamilNadu 4 endemic areas have been identified in the survey, (Madurai,Ramnad, Rajapalayam, and Sivaganga). The common denominator in these areathe habit of people taking bath in common ponds.

Theories of mode of spread:1. Demellow's theory of direct transmission


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2. Autoinoculation theory of Karunarathnae (responsible for satellite lesions)3. Haematogenous spread - to distant sites4. Lymphatic spread - causing lymphadenitis (rarity)

Demellow's theory of direct transmission - This theory propounded by Demellow hacceptance for quite sometime. He postulated that infection always occured as a of direct transmission of the organsim. When nasal mucosa comes into contact wiinfected material while bathing in common ponds, infection found its way into the nmucosa.

Karunarathnae accounted for satellite lesions in skin and conjunctival mucosa as result of auto inoculation.

Rhinosporidiosis affecting distant sites could be accounted for only throughhaematogenous spread.

Karunarathnae also postulated that Rhinosporidium existed in a dimorphic state. Iexisted as a saprophyte in soil and water and it took a yeast form when it reachedinside the tissues. This dimorphic capability helped it to survive hostile environmefor a long period of time.

Reasons for endemicity of Rhinosporidiosis:

It has to be explained why this disease is endemic in certain parts of South India athe dry zone of Srilanka. If stagnant water could be the reason then the chemical aphysical characteristics of the water needs to be defined. In addition other aquaticorganisms may also be playing an important synergistic reaction. This aspect neebe elucidated. Text book of microbilogy is repleate with examples of such synergisi.e. lactobacillus with trichomonas, and Wolbachia with filarial nematodes.

Host factors responsible for endemicity: Eventhough quite a large number of peopliving in the endemic areas take bath in common ponds only a few develop the

disease. This indicates a predisposing, though obscure factors in the host. Blood gstudies indicate that rhinosporidiosis is common in patient's with group O (70%), tnext high incidence was in group AB. Jain reported that blood group distribution isvariable to draw any conclusion. Larger series must be studied for any meaningfuanalysis. HLA typing also must be studied. The possibility of non-specific immunereactivity especially macrophages in protecting the individual from Rhinosporidiumseeberi must be considered.

Life cycle: (Ashworth) Spore is the ultimate infecting unit. It measures about 7 micabout the size of a red cell. It is also known as a spherule. It has a clear cytoplasm

15 - 20 vacuoles filled with food matter. It is enclosed in a chitinous membrane. Thmembrane protects the spore from hostile environment. It is found only in connecttissue spaces and is rarely intracellular.

The spore increases in size, and when it reaches 50 - 60 microns in size granulesstarts to appear, its nucleus prepares for cell division. Mitosis occurs and 4, 8, 16,and 64 nuclei are formed. By the time 7th division occurs it becomes 100 micronssize. A fully mature sporangia measures 150 - 250 microns. Mature spores are fouthe centre and immature spores are found in the periphery.


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The full cycle is completed within the human body.

Figure showing life cycle(old) of Rhinosporidium Seeberi

Life cycle (recent): Since rhinosporidium seeberi has defied all efforts to culture it,detail regarding its life cycle will have to be taken with a pinch of salt. This life cycbeen postulated by studying the various forms of rhinosporidium seen in infected

tissue.

Trophozoite / Juvenile sporangium - It is 6 - 100 microns in diameter, unilamellar, positive with PAS, it has a single large nucleus, (6micron stage), or multiple nuclemicrons stage), lipid granules are present.

Intermediate sporangium - 100 - 150 microns in diameter. It has a bilamellar wall, chitinous and inner cellulose. It contains mucin. There is no organised nucleus, lipglobules are seen. Immature spores are seen within the cytoplasm. There are nomature spores.

Mature sporangium - 100 - 400 microns in diameter, with a thin bilamellar cell walInside the cytoplasm immature and mature spores are seen. They are foundembedded in a mucoid matrix. Electron dense bodies are seen in the cytoplasm. Tbilamellar cell wall has one weak spot known as the operculum. Maturation of spooccur in both centrifugal and centripetal fashion. This spot does not have chitinouslining, but is lined only by a cellulose wall. The mature spores find their way out ththis operculum on rupture. The mature spores on rupture are surrounded by mucomatrix 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 u


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c. Benign tumors of larynx: Initially benign tumors of larynx included even

inflammatory disorders involving the vocal folds like vocal nodule, vocal cord poly

In 1950's definition of benign tumors of larynx under went a sea change. It exclu

all inflammatory conditions of larynx while concentrating on true benign tumors

instead. Inflammatory disorders involving vocal cords were classified under pseu

tumors (tumor like condition).

Studies have shown that true benign tumors involving larynx are pretty rare.

Pathological classification of benign laryngeal tumors:

This is based on the tissue of origin. They have been grossly divided into epithel

and non epithelial.

Epithelial tumors:


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Benign tumors involving the larynx can be excised without compromising the

functional status of larynx.

d. Labyrinthitis:

Introduction: This is defined as an inflammatory disorder involving the inner ear /

labyrinth. Clinically this condition causes disturbances of balance and hearing ofvarying degrees in the involved ear.

Causes:

1. Bacterial infections

2. Viral infections

3. Autoimmune causes

4. Vascular ischemic causes

Pathophysiology:

Anatomically labyrinth is composed of an outer osseous framework surrounding t

delicate membranous labyrinth which contains the peripheral end organs of hear

and balance. Membranous labyrinth include:

1. Utricle

2. Saccule

3. Semicircular canals

4. Cochlea

The labyrinth lies within the petrous portion of temporal bone. It communicates w

the middle ear via the oval and round windows.

Infecting organism may find their way into the inner ear via:1. Pre-existing fractures

2. Oval window

3. Round window

4. Congenital dehiscence involving the bony labyrinth

Viral labyrinthitis: Is characterized by sudden unilateral loss of hearing and

equilibrium. Vertigo is usually incapacitating and associated with vomiting. Thes

patients are bed ridden. Vertigo usually subsides within 4-6 weeks. Hearing loss

confined to high frequencies and is sensorineural in nature. An attack of upperrespiratory tract infection precedes the development of labyrinthitis. This conditio

should not be compared with vestibular neuronitis which involves only the vestibu

nerves and spares the cochlear component. Varicella Zoster oticus is an unique

of viral labyrinthitis caused by reactivation of dormant varicella zoster virus. This

reactivated virus is known to attack spiral ganglion.

Common viral causes of labyrinthitis:

1. Mumps

2. Measles

3. Rubella (congenital labyrinthitis)


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4. Cytomegalovirus

Bacterial labyrinthitis: can be potentially caused by meningitis / otitis media. This

could be caused by direct invasion of membranous labyrinth by the infecting orga

(suppurative labyrinthitis) causing permanent destruction of vestibular and cochle

end organs. In patients with meningitis spread of infections can be bilateral since

infections can travel via the CSF and involve the inner ear fluids through the interacoustic meatus / cochlear aqueduct. Bacterial infections involving the middle ea

cavity can enter the labyrinth via erosion of lateral canal which is commonly seen

patients with cholesteatoma. Treatment is usually directed against infecting orga

and supportive therapy. Suppurative labyrinthitis is usually followed by labyrinthit

ossificans where the whole of the membranous labyrinth gets ossified. Labyrinth

ossificans indicates a permanently dead labyrinth.

Common bacterial causes of labyrinthitis include:

1. S. pnuemoniae

2. Haemophilus influenza

3. Streptococcus

4. Staphylococcus

5. Neisseria

6. Bacteroids

7. Proteus

8. Moraxella catarrhalis

Serous labyrinthitis:

This is a potentially reversible disorder caused by diffusion of bacterial toxins intoinner ear via the inflamed round window membrane. Studies have shown that th

permeability of the round window membrane is increased when there is inflamma

This may cause diffusion of bacterial toxins and immune mediators into the inner

causing transient impairment of the inner ear functions.

Autoimmune labyrinthitis:

This is an uncommon cause of sensorineural hearing loss. This may be caused

localized / general autoimmune reactions. Examples of general autoimmune diso

causing labyrinthitis include Wegener's granulomatosis and polyarteritis nodosa.

e. Seasonal allergic rhinitis: Rhinitis is defined as inflammation of nasal mucosa.

This condition is caused over reaction of immune system to inhaled allergen.

Seasonal rhinitis is commonly caused due to inhalation of pollen grains. It is also

known as the Hay fever. This is caused by outdoor allergens which are released

during flowering seasons (spring).

Symptoms:

Running nose

Nasal block


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Itching in the eyes

Mild pyrexia

Sneezing

Dark circles under the eyes

Post nasal drip

Reactions are usually mediated by release of Histamines due to the activation of in the nasal mucosa.

Common allergens responsible for seasonal allergic rhinitis include:

Rag weed Most common allergen

Grass pollen Common during late spring and early winter

Tree pollen Common in spring

Fungus

Patients with allergic rhinitis may also suffer from any of the following:

These are also known as co morbid conditions.

1. Asthma

2. Allergic dermatitis

3. Allergic sinusitis

4. Nasal polyposis

On examination:

Chronic allergic rhinitis patients will demonstrate:

Dark circles around the eyes. This is related to vasodilatation / nasal congestion

Hence these patients go by the name Allergic shiners.

Presence of nasal crease. This is a horizontal crease across the lower half of thebridge of the nose due to the upward repeated rubbing of the tip of the nose with

palm of the hand. This is known as Allergic salute.

Nasal examination:

Is best performed by using nasal speculum. The nasal mucosa in these patients

appear pale and boggy. The inferior turbinates are commonly enlarged in these

patients. Nasal mucous secretion is found to be thin and watery.

Management:

Environmental control measuresPharmacological agents

Immunotherapy: Also known as desensitization procedure. In this therapy the pa

is injected regular small doses of the allergen he is responsive to. Repeated inje

of the allergen is likely to desensitize the patient. The allergic response of these

patients to the allergen is not dramatic after immunotherapy.

Prevention:

Staying indoors during the season

Using air conditioners

Use of HPEA filter in the bedroom


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Medical management:

Antihistamines Commonly used are fexofenadine, cetrizine, and desloratidine.

Steroids in severe cases Steroids can be administered either systemically whic

a lot of undesirable side effects. Topical application of beclamethazone in the for

nasal spray has the double advantage of low dose steroid therapy and local actio

Mast cell degranulating agents (Montelukast) Histamines are released by

degranulation of mast cells. If the process of degranulation is blocked somehow

symptoms could become manageable.

If the nasal block is troublesome nasal decongestants (topical) can be used.

f. Investigations for dysphagia:

Conventional investigations of dysphagia include:

Barium swallow:

This is a contrast radiological investigations in which the patient is asked to swall

contrast agent i.e. barium and serial x-rays are taken. This investigation helps in

identifying the site of the probable lesion if there is any obstructive pathology is

involved. It gives a clear view of pyriform fossa, post cricoid region and oesopha

Usually barium swallow indicates the probable site of the mass lesion. It is very

in identifying obstructing mass lesions.

Upper GI endoscopy:

This is usually performed using a flexible endoscope. The whole of the upper

digestive tract can be visualized. Biopsy can be taken from suspicious looking leDynamic obstruction in the oesophagus causing dysphagia can be identified only

performing oesophageal manometry.

X-ray Chest PA: This will reveal compressing lesions like enlarged mediastinal no

enlarged right atrium. If chest radiology reveals any abnormality then the patient

should be subjected to CT scanning in order to clinch the diagnosis.

Plain x-ray soft tissue neck AP / Lateral view: Will reveal the presence of foreign

bodies at the level of cricopharynx. It will also reveal widening in the prevertebra

area caused by retropharyngeal abscess / malignancy involving the post cricoidregion.

Swallowing electromyography:

This is really helpful in real time assessment of swallowing disorders. Neuromus

swallowing defects can easily be picked up. It is very useful in identifying

neuromuscular swallowing disorders in infants and children.

Videofluroscopy swallow study:

This study really helps in identifying the causes of dysphagia. Video recordings a

made while the patient is attempting to swallow. Various stages of swallowing ca

clearly recorded and analyzed. It also reveals the presence of aspiration into


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the airway if present. Structural movements that can be assessed in this examia

include:

1. Lips

2. Tongue

3. Jaw

4. Soft palate5. Pharyngeal walls

6. Hyoid bone

7. Epiglottis

8. Thyroid cartilage

9. Arytenoids

10. Upper esophageal sphincter

Respirodeglutometry:

During the process of deglutition there is apnoea. By studying the respiratory pa

during deglutition abnormalities if any can be identified. The respirodeglutometer

contains a respiratory channel which is capable of recording information regardin

flow of air and its cessation during the process of deglutition.

Short answers: 10x2 = 20 marks

1. Ludwigs angina: Ludwigs angina is described as rapidly spreading cellulitis

involving the floor of the mouth. It was first described by Wilhelm Friedrich von Lu

in 1836. This disorder has a potential for airway obstruction. It is commonly causdue to dental infections.

2. Tracheostomy: The word tracheostomy is derived from the greek word trach

plus stoma (mouth). This procedure involves creating an opening in the anterior w

trachea with suturing of the skin of the neck with the tracheal mucosa. A tube is

inserted through this stoma (opening) to facilitate respiration. Indications for

tracheostomy include: a. Upper airway obstruction above the level of vocal cords

b. For assisted ventilation

c. Bronchial toiletingd. Prolonged intubation to prevent tracheal stenosis

3. Laryngomalacia: The term Malakia in Greek means softening. The term

indicates softening of larynx. This is a disease of infants and children. This diseas

characterised by the presence of stridor which is caused due to excessive redund

of supraglottic tissues which gets sucked into the glottis due to the negative press

caused during inspiration. The stridor in these patients are inspiratory in nature.

is a self limiting disorder which resolves as the child grows older


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4. Osteomeatal 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 anterigroup of ethmoidal air cells. It is through this area that the anterior group of sinus

drain. Obstructions involving this area can lead to chronic sinusitis.

5. Sphenoid sinus: Is located in the skull base at the junction of the anterior an

middle cranial fossa. Pnematisation of sphenoid starts during the 4th year of child

and gets completed by the 17th year. The sphnoid sinuses vary in size and may b

asymmetric. They drain through the superior meatus via a small ostium about 4m

diameter located disadvantageously 20mm above the sinus floor. This sinus is re

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 wal

The nerve of pterygoid canal lie in the floor of the sinus. Hence infections of sphe

sinus may involve the optic nerve if the canal of the optic nerve is dehiscent.

6. Parapharyngeal space:The parapharyngeal space is a potential deep neck

space, is also known as pterygomaxillary space, pharyngomaxillary space,or late

pharyngeal space. It is more or less shaped like an inverted pyramid with the ba

pointing towards the skull base and the apex towards the hyoid bone. Its boundaare as follows:

Medial: It is bounded by the naso and oropharynx

Anterolateral: Bounded by the masticator space

Posterolateral: Bounded by the deep lobe of parotid gland

Posteromedial: Bounded by the retropharyngeal space

This space is filled with loose connective tissue, associated lymphatics, and nodeThe contents of the carotid sheath may also be considered to be part of the

parapharyngeal space.

7. Petrositis: Involvement of air cells around petrous apex causes a unqiue

syndrome known as Gradinego's syndrome. It is characterized by:

otorrhoea

Diplopia due to lateral rectus palsy due to involvment of 4 th cranial nerve at Dorol

canal

Retro orbital pain due to involvement of trigeminal nerve


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8. Otomycosis: Fungal infections of the external auditory canal are common c

of otitis external in the tropics. It is seen as whitish flakes (candida), black specs

(Aspergillus niger). Infections can also be mixed. Due to the presence of intense

itching patient has a tendency to use ear buds. This traumatizes the ear canal st

leading on to otitis externa.

9. Inverted papilloma:

The mucosal lining of nose and para nasal sinuses is known as

Schneiderian membrane, in memory of Victor Conrod Schnider who described

histology. Papillomas arising from this membrane is very unique in that they are

to be growing inwardly and hence the term inverted papilloma. These papillomas

unique in their history, biology and location.

10. Caloric tests: Are simple bed side tests performed to ascertain vestibular fun

These include:

Caloric test: The classic bithermal caloric test is preformed with both warm and

water. The warm water's temperature should be 7 degrees above normal body

temperature and the cold water temperature should be 7 degrees below normal b

temperature in order to optimally stimulate the labyrinth. The volume of water to binjected is about 250 ml and the irrigation is performed for about 30 seconds. Dur

caloric test the lateral canal is stimulated. While water is being irrigated in to the

the eyes are looked for the presence or absence of nystagmus. Absence of

nystagmus indicate dead labyrinth. The pnemonic COWS helps one to remembe

direction of nystagmus.

Cold opposite side

Warm same side

Cold caloric test: Also known as Kobracks test. This is used as a rapid caloric teOnly the cold water is used to perform this test.

Documents

Tamil Nadu Dr MGR Medical University ENT MBBS Prefinal Feb 2009 question paper with solution