mgr medical university ms ent basic sciences march 2009 question paper with solution

8/8/2019 MGR medical university MS ENT basic sciences march 2009 question paper with solution

1/44

www.drtbalu.co.in

The Tamilnadu Dr MGR Medical University MS (ENT)

Basic sciences

Question paper March 2009 with solutions

By

Dr. T Balasubramanian


2/44

www.drtbalu.co.in

MS (ENT) Applied Basic Sciences

March 2009

I. Anatomy: Answer any fourFacial recess Is defined as an aerated extension posterior superior

portion of the middle ear cavity medial to the tympanic annulus and

lateral to the fallopian canal.

Boundaries:

Medial Facial nerveLateral Tympanic annulus

Superior Incus buttress (near the short process of incus)

Running through the wall between these two structures with varying

degrees of obliquity is the chorda tympani nerve. Chorda tympani

nerve always run medial to the tympanic membrane.

Drilling in this area between the facial nerve and annulus in the angle

formed by the chorda tympani nerve leads into the middle ear cavity.

This surgical approach to the middle ear cavity is known as facial

recess approach.

Uses of facial recess approach:

1. Used to reach hypotympanum of middle ear2. Used to place cochlear implant electrode into the cochlea via the

round window.

3. Horizontal portion of facial nerve can be accessed via thisapproach. Hence this approach can be used to performdecompression of horizontal division of facial nerve.


3/44

www.drtbalu.co.in

Occasionally cholesteatoma of middle ear cavity can invade the

mastoid antrum without involving the aditus. It has been

hypothesized that drilling this area can provide additional avenue for

mastoid aeration.

Land marks used to identify this region:

1. External genu of facial nerve medially


4/44

www.drtbalu.co.in

2. Fossa incudes superiorly3. Chorda tympani laterally4. Tympanic membrane anteriorly and laterally.

Trautmans triangle:

This is a triangular space bounded by

Bony labyrinth anteriorly

Sigmoid sinus posteriorly

Dura containing superior petrosal sinus superiorly.

This triangle is a potential weak spot through which infections of

temporal bone may traverse and affect cerebellum. Extra duralabscess involving the posterior cranial fossa is also possible when thin

bone in this triangle gets breached in infections / cholesteatoma

involving mastoid cavity.

Since bone in this area is rather thin it can be drilled out to enter into

the posterior cranial fossa. This can be used as an approach to

posterior cranial fossa lesions.

The size of this triangle is highly variable depending on the size of the

sigmoid sinus. A large sigmoid sinus reduces the size of this triangle

and also increases the angulation of the superior petrosal sinus with

it. This impedes the venous drainage predisposing to the

development of endolymphatic hydrops.


5/44

www.drtbalu.co.in

Recurrent laryngeal nerve:

Introduction:

In order to understand the various neurological problems affecting

the mobility of the vocal cord a clear understanding of the anatomy

of recurrent laryngeal nerve is a must because it supplies the muscles

acting on the vocal cord. The larynx is intimately involved in

swallowing, breathing, coughing and phonation. These functions are

dependent on normal movements of the vocal cords. These

movements are controlled by muscles which are innervated by

therecurrent laryngeal branch of the vagus nerve.

Anatomy: The recurrent laryngeal nerve is a myelinated nerve. It is a

component of the vagus nerve. As the vagus nerve exits the medulla,the fibers of the recurrent laryngeal nerve are anteriorly situated in

it. As the vagus traverses inferiorly, the fibers of the recurrent

laryngeal nerve starts to rotate medially until they are ultimately

separated from the vagus 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 recurrent

laryngeal nerve arising from the vagal nerve just below the aortic


6/44

www.drtbalu.co.in

arch loops medially under the aorta and ascends within the

tracheoesophageal groove. The anterior bronchoesophageal artery

supplies the left vagus nerve. The right vagus nerve descends with

the common carotid artery. At the level of division of the innominate

artery, the right recurrent laryngeal nerve loops around the

subclavian artery and ascends along the superior lobe of the pleura. It

then approaches the tracheoesophageal groove behind the common

carotid artery. The approximate length of the left recurrent laryngeal

nerve is 12 cms, whereas the right nerve measures about 6 cms only.

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. The right recurrent laryngeal nervedoes not get into the tracheoesophageal groove until it approaches

the cricothyroid joint. In some patients the right recurrent laryngeal

nerve is given off from the vagus nerve at the level of thyroid gland,

this condition is always associated with an anomalous

retroesophageal location of the right subclavian artery. This is also

known as anon recurrent variationof the right recurrent laryngeal

nerve. This condition places the nerve at risk during thyroid surgery.


7/44

www.drtbalu.co.in

Diagram showing the right and left recurrent laryngeal nerves

Relationship of recurrent laryngeal nerve with inferior thyroid artery:

The recurrent laryngeal nerve has significant but varying relationship with

the inferior thyroid artery. On the left side, the recurrent laryngeal nerve passesbehind 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. On the right side since the recurrent laryngeal nerve

approaches the tracheoesophageal groove more laterally, these relations are

different on the right side. In half of the cases the recurrent laryngeal nerve

passes between the distal branches of the inferior thyroid artery, in 30% ofpatients it may lie anterior to the artery, and in 20% of cases it may lie deep tothe inferior thyroid artery.

The recurrent laryngeal nerve enters the larynx deep to the inferior constrictor

muscle and posterior to the cricoarytenoid joint. Inside the larynx it divides into

sensory and motor branches. The anteriorly directed motor branch is made up of

1000 axons. About 250 of the axons innervate the cricoarytenoid muscle, since

it is the sole abductor of the vocal fold. The trachea, oesophagus and pyriform

sinuses receive their sensory fibers from the posterior division of the recurrentlaryngeal nerve before entering the larynx.


8/44

www.drtbalu.co.in

The blood supply to the recurrent laryngeal nerve comes from the inferior

thyroid artery. The feeding branches are usually anterior to the nerve. Distally,

the inferior laryngeal artery, a terminal branch of the inferior thyroid artery,supplies the recurrent laryngeal nerve.

Figure showing left recurrent laryngeal nerve and its course

The pretracheal fascia that covers the thyroid gland condenses and attaches

the thyroid gland to the upper two tracheal rings is known as the Berry'sligament. The recurrent laryngeal nerve often passes through this layer to

enter the larynx.


9/44

www.drtbalu.co.in

Figure showing the relationship between recurrent laryngeal nerve and

Berrys ligament


10/44

www.drtbalu.co.in

Uncinate process:

The uncinate process is a wing or boomerang shaped piece of bone. It

forms the first layer or lamella of the middle meatus. It attaches

anteriorly to the posterior edge of the lacrimal bone, and inferiorly to

the superior edge of the inferior turbinate. Superior attachment of

the uncinate process is highly variable, may be attached to the lamina

papyracea, or the roof of the ethmoidal sinus, or sometimes to the

middle turbinate. The configuration of the ethmoidal infundibulum

and its relationship to the frontal recess depends largely on the

behaviour of the uncinate process. The uncinate process can beclassified into 3 types depending on its superior attachment. The

anterior insertion of the uncinate process cannot be identified clearly

because it is covered with mucosa which is continuous with that of

the lateral nasal wall. Sometimes a small groove is visible over the

area where the uncinate attaches itself to the lateral nasal wall.

Figure showing Type I uncinate process

Type I uncinate: Here the uncinate process bends laterally in its upper most

portion and inserts into the lamina papyracea. Here the ethmoidal


11/44

www.drtbalu.co.in

infundibulum is closed superiorly by a blind pouch called the recessus

terminalis (terminal recess). In this case the ethmoidal infundibulum and the

frontal recess are separated from each other so that the frontal recess opens

in to the middle meatus medial to the ethmoidal infundibulum, between the

uncinate process and the middle turbinate. The route of drainage and

ventilation of the frontal sinus run medial to the ethmoidal infundibulum.

Figure showing type II uncinate process

Type II uncinate: Here the uncinate process extends superiorly to the roof of

the ethmoid. The frontal sinus opens directly into the ethmoidal infundibulum.

In these cases a disease in the frontal recess may spread to involve the

ethmoidal infundibulum and the maxillary sinus secondarily. Sometimes the

superior end of the uncinate process may get divided into three branches one


12/44

www.drtbalu.co.in

getting attached to the roof of the ethmoid, one getting attached to the lamina

papyracea, and the last getting attached to the middle turbinate.

Figure showing type III uncinate process

Type III uncinate process: In this type the superior end of the uncinate process

turns medially to get attached to the middle turbinate. Here also the frontal sinusdrains directly into the ethmoidal infundibulum.

Uncinate process should be removed in all endoscopic sinus surgical procedures

in order to open up the middle meatus. In fact this is the first step in endoscopicsinus surgery.


13/44

www.drtbalu.co.in

Rarely the uncinate process itself may be heavily pneumatised causing obstruction to the infundibulum.

Nasal tip supports:

Nose is the most prominent portion of face. It is also responsible for the

aesthetics of the face. Surgical increase / decrease of projection of nasal tip in

relation to face play an important role in the success of rhinoplasty

procedures. Anatomically nasal tip area is very complex. Inadvertent damage

to the support structure of nasal tip area during surgery will cause disastrous

results.

Tripod theory of Anderson: This theory explains the nasal tip supporting

mechanisms. Anatomically the two alar cartilages form a functional tripod that

supports the nasal tip. The right and left lateral crura comprise the two legs of

the tripod, while the two conjoined medial crura forms the third leg. The apex

of the tripod is considered to be the tip of the nose. This tripod is supposed

to be the major support of nasal tip. Medial crura are shorter than the lateral

crura. Tip rotations can take place either due to increase in the length of

medial limb or decrease in the height of lateral limbs. These medial crura are

further supported by attachments to superior and inferior portions of nasal

septum. The nasal tip tripod is considered to be a dynamic unit suspended and

supported by surrounding rigid structures. Other major nasal tip supports

include:

1. The attachment of medial crural feet to the caudal end of quadrangularcartilage

2. Scroll like attachment of the caudal end of upper lateral cartilage to thecephalic margin of the lateral crura

Tardys classification of nasal tip support systems:

According to Tardy there are three major and six minor support mechanisms of

nasal tip.

Tardys major support mechanisms include:

1. Size, shape, strength and resilience of medial and lateral crura


14/44

www.drtbalu.co.in

2. Attachment of medial crural foot plate to the caudal border ofquadrangular cartilage

3. Attachment of upper lateral cartilages (caudal border) to alar cartilages(cephalic border).

The six minor support mechanisms are supposed to augment the major

support system.

Tardys Minor tip support system includes:

1. Ligamentous sling spanning the domes of alar cartilages2. Dorsal portion of cartilaginous nasal septum3. Sesamoid complex extending the support of lateral crura to the pyriform

aperture

4. Attachment of alar cartilage to the overlying skin and musculature5. Nasal spine6. Membranous portion of nasal septum

This classification of support systems of nasal tip is based on clinical experience

rather than anatomical models. According to Tardy the tip recoil mechanism

can be used to study the contribution made by these different nasal tip

support systems.

Janeke and Wright nasal tip support hypothesis:

This hypothesis proposes that fibrous connection between the upper and

lower lateral cartilages play a vital role in the nasal tip support mechanism.

This is in addition to the support structures suggested by Tardy. According to

Wright this fibrous connection between the upper and lower lateral cartilages

play a vital role in determining the nasal tip tripod structure.


15/44

www.drtbalu.co.in

Figure showing the nasal tip support structure

Figure showing the nasal tip tripod as viewed from below

II. Physiology: Answer any fourStapedial reflex:

The Stapedial muscle inserts into the head of stapes. When it

contracts it stiffens the ossicular chain mechanism. Contraction of

stapedius muscle increases the impedance of middle ear conduction


16/44

www.drtbalu.co.in

system thereby protecting the inner ear from the damaging effects of

high intensity sound.

If the hearing is normal a sound intensity level of 8o dB is sufficient to

evoke Stapedial reflex. Broad band sounds evoke Stapedial reflex at

sound pressure levels of 20dB level.

Stapedial reflex is usually bilateral. If sound is delivered to one ear

stapedius muscle on both sides contract via the acoustic facial reflex

arc. Reflex generated on the side of stimulation is known as

ipsilateral reflex (uncrossed reflex). Reflex generated on the opposite

side is known as crossed (contralateral reflex).

Stapedial reflex threshold Is defined as minimum sound pressure

level needed to produce measurable change in the tympanicmembrane impedance.

Ipsilateral reflex pathway:

Ipsilateral ear

cochlearnerve

Cochlearnucleus

Superiorolivary

complex

Facial nervenucleus

Facial nerve

StapediusMuscle


17/44

www.drtbalu.co.in

Contralateral reflex pathway:

Uses of Stapedial reflex measurements:

1. It provides an objective measurement of patients hearing levels2. Helps in identification of probable site of lesion in patients with

facial paralysis

3. Can identify malingerersComplete absence of Stapedial reflex may be due to:

1. Ossicular chain pathology2. Vestibular schwanomma3. Cochlear / retrocochlear deafness4. Brain stem lesions (multiple sclerosis, haemorrhage)5. Diseases involving facial nerve6. Diseases involving stapedius muscle (myasthenia gravis)

Contralateralear

Superior olivarycomplex

decussation

Contralateralsuperior olivary

nucleus

Contralateralfacial nerve

nucleus

Facial nerve

StapediusMuscle


18/44

www.drtbalu.co.in

7. To assess the pure tone threshold in a deaf mute child in order toselect a hearing aid.

8. In otosclerosis to select the ear for surgery.

Stapedial reflex testing protocol:

Ipsilateral testing: The probe ear is stimulated using tone pulses at

500- 4000 Hz or with broadband stimuli at sound pressure levels of 70-90dB

above the hearing threshold. The first recordable change in the impedance is

recorded as Stapedial reflex threshold level.

Contralateral testing: The same impedance recording is performed inthe opposite ear. Contralateral reflex is dependent on the integrity of superior

olivary complex decussation.

Advantages of acoustic reflex threshold estimation:

1. It is an objective test2. Non invasive3. Assess middle ear function accurately4. It is possible to test children5. Malingering can easily be detected.

How to perform this test?

1. Patient should be alerted that loud sounds will he heard in eitherear. They should be advised to sit quietly and calmly.

2. The immitance probe is placed in the ear canal that is to be tested(probe used for tympanometry). The contralateral probe shouldbe placed in the opposite ear.

3. Tympanometry is performed first. This is a must because acousticreflexes should be measured with the ear canal pressure set to

obtain the maximum compliance for 226Hz probe tone.

4. It is not advisable to go above 105dB sound pressure level unlessthe patient has conductive deafness


19/44

www.drtbalu.co.in

5. Tones are presented to the test ear at 0.5, 1, 2, and 4 kHzfrequencies at 70-80dB sound pressure level in 5dB increments till

acoustic reflex is obtained.

6. If the tone presented is loud enough to evoke Stapedial reflex theimmitance probe will record it.

7. It should be ensured that the reflex is a true one and not anartefact by repeating the test at the same frequency and sound

pressure levels.

Theories of hearing:

There are various theories attempting to explain how sounds are

perceived by the brain. The following are the commonly proposed

theories:

Place theory:

This theory was proposed by Hermann Helmholtz. This theory is

based on the assumption that pitch discrimination takes place at the

level of cochlea. Helmholtz was able to demonstrate that the basal

turn of cochlea responded best to high frequency sounds while the

apical portion of cochlea responded better to low frequency sounds.

He assumed that the middle portion of the cochlea responded to

various middle frequency sounds. He considered the basilar

membrane to be tuned like a string of a piano. When sound reaches

the ear the various frequencies stimulate various portions of thebasilar membrane playing a role in pitch discrimination. Experiments

particularly the present day ones have not categorically proved that

pitch discrimination occurs at the level of cochlea, it has to be

accepted that certain amount of gross pitch discrimination takes

place at the level of cochlea.

Telephone theory (Pitch theory):

This theory was proposed by Rutherford. This theory suggests that

pitch discrimination takes place at the level of auditory nerves.


20/44

www.drtbalu.co.in

According to this theory all portions of the basilar membrane are

stimulated by every frequency and the pitch perception depends on

the number of times the auditory nerve fibers discharge. Studies

have demonstrated that maximal discharge rate of auditory nerve

fibers is 1000/sec. This indicates that pitch discrimination of

frequencies above this frequency cannot be perceived hence this

theory is also not a complete explanation of sound perception by

brain.

Volley theory:

This theory was proposed by Weaver. This theory is a judicial

combination of place theory and telephone theory. Perception of

sound with frequencies up to 5000Hz depends on the firing rate ofauditory nerves (pitch theory) and frequencies above 5000 Hz

depends on maximal excitation of various portions of cochlea (place

theory).

Travelling wave theory of Bekesy:

This is one type of place theory. This theory holds that pitch

discrimination is determined when a certain place along the basilar

membrane is set into maximum vibration. The auditory nerve fibers

supplying the maximally vibrating portion of basilar membrane start

to fire in response to it.

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 toyogis 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.


21/44

www.drtbalu.co.in

Nasal secretions are also cyclical. Secretions are found to be

increased on the side with the greatest airflow.

Factors that modify nasal cycle:

1. Allergy2. Infection3. Exercise4. Hormones5. Pregnancy6. Fear / emotions7. Sexual activity8. High levels of CO2 in the inspired air causes a reduction in the

nasal resistance

9. Drugs that block the action of noradrenaline cause reduction inthe nasal cycle.

The reason for nasal cycle still remains to be studied.

Mechanism of speech:

Speech process involves:

1. Speech centres in the brain2. Respiratory centre in the brainstem3. Respiratory system4. Larynx5. Pharynx6. Nose / nasal cavities/sinuses7. 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 Wernickes area of brain. This involves input

from visual and auditory areas. From this area stimuli are sent to Brocas area

where vocalization control is located.


22/44

www.drtbalu.co.in

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 beadjusted 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 Bernoullis effect. Bernoullis 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.


23/44

www.drtbalu.co.in

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. Lips2. Jaw3. Teeth4. Different regions of tongue5. Gum ridge6. Hard palate7. Soft palate8. 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.


24/44

www.drtbalu.co.in

Circulation of CSF:

Cerebrospinal fluid is present between the arachnoid and piamater.

Production:

CSF is produced from arterial blood by the choroid plexuses of lateral

and 4th

ventricles. Actual production of CSF is by a combination of

diffusion, pinocytosis and active transfer. A small amount of CSF is

produced by ependymal cells.

Total volume of CSF in an adult is 140 ml. CSF is produced at a rate of

0.2 0.7 ml /min. Total production ranges about 600 / 700 ml/day.

The circulation of CSF is aided by the pulsations of the choroid plexus

and by the motion of the cilia of ependymal cells. CSF is absorbedacross the arachnoid villi into the venous circulation. The arachnoid

villi act as one-way valves between the subarachnoid space and the

dural sinuses. The rate of absorption correlates with the CSF

pressure.

CSF circulates from the lateral ventricles through foramen Munroe

into the third ventricle. From third ventricle it traverses the aqueduct

of sylvius to the 4th

ventricle. From the 4th

ventricle reaches the

subarachnoid space via foramen of Lushka and Megnedie. CSF

returns back to the vascular system by entering the dural venous

sinuses by reabsorption via arachnoid granulations. CSF is also

known to flow along cranial and spinal nerve roots from where it may

be absorbed via lymphatic channels to reach venous circulation.

Circulation of CSF is facilitated by:

1. Hydrostatic pressure during its production2. Arterial pulsations3. Directional beating of ependymal ciliaCSF acts as a cushion that protects the brain from shocks and

supports the venous sinuses. It also plays an important role in the

homeostasis and metabolism of the central nervous system.


25/44

www.drtbalu.co.in

Figure showing CSF circulation

III. Biochemistry: Answer any threeEndolymph analysis:

Among the extracellular fluids present in the body, endolymph has a

unique ionic composition. It has a low sodium content and high

potassium content.

Endolymph is produced by marginal cells of stria vascularis. The

following enzymes have also been demonstrated in the

endolymphatic fluid:

1. Sodium potassium ATPase2. Adenyl cyclase3. Carbonic anhydrase


26/44

www.drtbalu.co.in

These enzymes play a vital role in maintaining the ionic concentration

of endolymphatic fluid. Maintenance of ionic concentration is vital for

maintenance of normal endocochlear potential. Glucose concentration in the

endolymphatic fluid mirrors that of plasma. Cells of the stria vascularis obtain

nourishment from endolymphatic fluid.

Metabolic alkalosis:

In metabolic alkalosis pH of blood is elevated beyond the normal

range (7.35-7.45). This is usually caused by a decrease in the

hydrogen ion concentration which causes an increase in the levels of

bicarbonate leading on to alkalosis. Direct increase in the

concentration of bicarbonate also will lead to metabolic alkalosis.

Two organ systems are commonly involved in the genesis of

metabolic alkalosis i.e. Kidneys and GI tract.

Pathogenesis: of metabolic alkalosis involves two processes i.e.

generation of metabolic alkalosis and the maintenance of the same.

Both these phases tend to overlap.

Generation of metabolic alkalosis occurs with either loss of acid or

gain of alkali. Sometimes, contraction of extracellular fluid

compartment with a consequent change in bicarb concentration canlead to metabolic alkalosis.

Role of kidneys:

Kidneys have enormous capacity to excrete excess bicarbonate in

order to restore normal pH in patients with metabolic alkalosis.

Kidneys make this possible by increasing the excretion of bicarbonate

ions as well as by reducing its reabsorption.

Metabolic alkalosis can be generated by any of these four

mechanisms:

1. Loss of hydrogen ions: When hydrogen ion is excreted,bicarbonate ion gets gained into extracellular space. Loss of

hydrogen ion can occur via the kidneys or GI tract. Vomiting /

nasogastric suction may induce metabolic alkalosis by excessive

loss of gastric hydrochloric acid. Renal excretion of hydrogen ions

may occur when sodium concentration increases in the distal

convoluted tubule due to increasing levels of aldosterone.


27/44

www.drtbalu.co.in

2. Shift of hydrogen ions into intracellular space: This invariablydevelops with hypokalaemia. As extracellular concentration of

potassium decreases, potassium ions move out of cells. To

maintain neutrality hydrogen ions move in to the intracellular

space.

3. Alkali administration: Administration of sodium bicarbonate inamounts that exceed the capacity of the kidneys to excrete this

excess bicarbonate may cause metabolic alkalosis. This capacity is

reduced when a reduction in filtered bicarbonate occurs, as

observed in renal failure, or when enhanced tubular reabsorption

of bicarbonate occurs, as observed in volume depletion.

4. Contraction alkalosis: This is associated with contraction ofextracellular fluid. Loss of bicarbonate-poor, chloride-rich

extracellular fluid, as observed with thiazide diuretic or loop

diuretic therapy or chloride diarrhoea, leads to contraction of

extracellular fluid volume. Because the original bicarbonate mass

is now dissolved in a smaller volume of fluid, an increase in

bicarbonate concentration occurs. This increase in bicarbonate

causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration.

Maintenance of metabolic alkalosis:

The following factors are responsible in the maintenance of metabolic

alkalosis.

1. Decrease in renal perfusion2. Stimulation of Renin angiotensin mechanism

Most common causes of metabolic alkalosis are:

1. Use of diuretics2. External loss of gastric secretions

Types of metabolic alkalosis can be divided into:

Chloride responsive alkalosis (urine chloride 20mEq/L)


28/44

www.drtbalu.co.in

Causes of chloride responsive alkalosis (urine chloride


29/44

www.drtbalu.co.in

Nasal crusts:

Crusts are whitish plaques seen in the nasal mucous membrane.

These crusts when removed leaves behind a bleeding base.Crusting involving nasal cavity is commonly caused by increased

drying of nasal mucous membrane / infections involving nasal

mucosa.

Common causes of crusts in the nasal cavity:

1. Infections tuberculosis / syphilis /diphtheria2. Atrophic rhinitis Crusts are greenish and foul smelling3. Extensive surgeries involving nasal mucosa4. Gross deviations of nasal septum causing directional changes in

the nasal airway causing drying and crusting of nasal mucosa.

5. Exposure to toxins like chromium6. Wegeners granuloma of nose

Histology:

When crusting of nasal mucosa occurs the area is covered with dried

nasal secretions and the normal ciliated columnar epithelium gets transformedinto keratinized squamous epithelium.

These crusts can be removed by moistening the nasal mucosa by using saline

irrigation.

IV. Pharmacology: Answer any threeAminoglycosides:

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.


30/44

www.drtbalu.co.in

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 ototoxic2. Nephrotoxic3. Neurotoxic in high doses

These drugs are used to treat predominantly gram negative

infections.

Chemicals used for cautery:

Many chemicals are known to cause tissue destruction. This property

can be made use of in stopping bleeding from anterior nasal cavities.

This procedure is known as chemical cautery. Sometimes chemical

cautery can be used to freshen the edges of tympanic membrane

perforation stimulating tissue overgrowth over the edges of

perforation leading to closure of perforation.

Drugs used in chemical cautery include:

1. Silver nitrate2. Copper sulphate3. Tricholoroacetic acid4. Cantheridin


31/44

www.drtbalu.co.in

Topical steroids:

These are topical forms of steroid preparations. These are used to

treat skin disorders. Topical steroid preparations are preferred for

their anti-inflammatory properties.

Nasal administration of topical steroid in aerosol form is preferred in

the management of allergic rhinitis.

Weak concentrations of topical steroids are used in disorders

involving eyes, facial skin, body folds, axillae, groin etc.

Advantages of topical administration of steroids:

This route of administration does not affect the pituitary axis. Dose

of steroid used is much below toxic limits of the drug. When

administered as nasal spray its dose is metered and is about 100

micrograms per puff. It has impressive topical effects while systemic

absorption is very minimal and hence does not cause Cushings

syndrome.Another important topical use of steroids is in the management of

bronchial asthma. It is delivered to the site of action (bronchioles) by

means of metered aerosol spray.

Soft steroids:

Topical steroids belonging to this group have very low incidence of

side effects but excellent anti-inflammatory properties. Drugs

belonging to this group include:

Hydrocortisone aceponate

Hydrocortisone buteprate

Methylprednisolone aceponate

Lignocaine:

This is an amino amide type of local anaesthetic. It is used as:

1. Topical anaesthesia2. Infiltrative anaesthesia


32/44

www.drtbalu.co.in

For topical anaesthesia it is used in 4% / 10% concentrations. 4%

xylocaine is used to anesthetize nasal mucosa. The topical anaesthesia lasts

for about 30 minutes. If mixed with adrenaline its anaesthetic effect could be

safely prolonged up to 1.5 hours. 10% xylocaine spray is used while

performing upper GI endoscopy procedures.

For infiltrative anaesthesia xylocaine should be administered in doses of 1-2%

concentration. Infiltrative anaesthesia is commonly used in nasal and ear

surgeries in otolaryngology. In this concentration the effect lasts for about 1

hours. If mixed with adrenaline its effect can be prolonged to about 3 hours.

Xylocaine acts by blocking neuronal conduction by blocking the fast gated

sodium channels. This blockage will prevent pain signals from propagating to

the brain.

V. Pathology: Answer any threePathology of meningioma:

Meningiomas are usually globular and well demarcated neoplasms.

They have wide dural attachment and may become invaginated into

brain without involving it. They are gritty on being sectioned. Cut

section of meningioma is usually pale / reddish brown in color. Some

meningiomas occur as a sheetlike extension that covers the dura but

does not invaginate the parenchyma; this variant is called

meningioma en plaque. The last morphologic variant is the cavernoussinus meningioma that infiltrates the cavernous sinus and becomes

interdigitated with its contents. The 3 most common histologic

subtypes of meningiomas are the meningothelial (syncytial),

transitional, and fibroblastic meningiomas. See images below for

representative pathologic views of various subtypes.

Meningothelial meningiomas reveal densely packed cells that are

arranged in sheets with no clearly discernible cytoplasmic borders. Although


33/44

www.drtbalu.co.in

not prominent, whorls are present (calcified whorls are termed psammoma

bodies). Nuclei show intranuclear vacuoles.

Fibroblastic (fibrous) meningiomas reveal sheets of interlacing spindle cells.

The intercellular stroma is composed of reticulin and collagen. The transitional

variety reveals features common to both the meningothelial and fibroblasticvarieties; others include angiomatous, microcystic, secretory, clear cell,

choroid, lymphoplasmacyte-rich, papillary, and metaplastic variants.

Meningiomas may be associated with hyperostosis. The exact nature of the

cause of this hyperostosis is controversial (ie, reactive versus tumoral

infiltration).

Immunohistochemistry:

Immunohistochemistry can help diagnose meningiomas, which are positive for

epithelial membrane antigen (EMA) in 80% of cases. They stain negative for

anti-Leu 7 antibodies (positive in schwannomas) and for glial fibrillary acidic

protein (GFAP). Progesterone receptors can be demonstrated in the cytosol of

meningiomas; the presence of other sex hormone receptors is much less

consistent. Somatostatin receptors also have been demonstrated consistently

in meningiomas.

Vasovagal attack:

This condition is caused by over activity /excessive stimulation of

vagus nerve. This condition is also known as Neurocardiogenic

syncope. This condition is more common in females.

Mechanism of vasovagal attack:

When vagus is stimulated the impulses reach the nucleus solitaries

present in the brain stem. Stimulation of this nucleus enhances

parasympathetic tone while inhibiting the sympathetic tone. Thisleads to a variety of hemodynamic responses which include:

1. Inhibition of cardiac muscle This leads to negative chronotrophiceffect causing a drop in the heart rate. The contractility of the

cardiac muscle is also reduced there by causing a reduction in the

cardiac output. This causes loss of consciousness.

2. Vasodepressor response This results in vasodilatation leading toa gross reduction in the blood pressure of the individual causing


34/44

www.drtbalu.co.in

unconsciousness. The heart rate could be normal in these

patients.

3. Majority of people could have a mixture of both cardiac andvascular phases of depression.

Signs & symptoms:

1. Weakness2. Visual disturbances3. Sweating4. Nausea5. Low blood pressure6. Slow heart rate7. Fainting

Triggers of vasovagal attacks:

1. Prolonged standing / upright sitting2. Standing up very quickly3. Stress4. Painful unpleasant stimuli5. Sudden emotional disturbances6. Abdominal straining7. Hyperthermia8. Pressing down on throat / eyes etc.9. High altitude10.Drug induces

Tests for diagnosis of vasovagal attacks:

Tilt table test

Holter monitoring

Electrophysiolic studies

Echocardiogram


35/44

www.drtbalu.co.in

Treatment:

1. Avoiding provoking stimuli2. Increase consumption of salt and fluids3. Voluntary tightening of leg muscles by crossing / uncrossing legs4. In acute cases Beta blockers and steroids will be helpful

Histopathology of atrophic rhinitis:

Pathologically atrophic rhinitis has been divided into two types:Type I: is characterised by the presence of endarteritis and periarteritis

of the terminal arterioles. This could be caused by chronic

infections. These patients benefit from the vasodilator effects of

oestrogen therapy.

Type II: is characterised by vasodilatation of the capillaries, these

patients may worsen with estrogen therapy. The endothelial cells lining

the dilated capillaries have been demonstrated to contain more

cytoplasm than those of normal capillaries and they also showed

a positive reaction for alkaline phosphatase suggesting the presence of

active bone resorption. It has also been demonstrated that a majority

of patients with atrophic rhinitis belong to type I category.

Once the diagnosis of atrophic rhinitis is made then the etiology should

be sought. Atrophic rhinitis can be divided in to two types clinically:

1. Primary atrophic rhinitis - the classic form which is supposed to arise

denovo. This diagnosis is made by a process of exclusion. This type of

disease is still common in Middle East and India. All the known causes

of atrophic rhinitis must be excluded before coming to this

diagnosis. Causative organisms in these patients have always been

Klebsiella ozenae.

2. Secondary atrophic rhinitis: Is the most common form seen in

developed countries. The most common causes for this problem could

be:


36/44

www.drtbalu.co.in

1. Extensive destruction of nasal mucosa and turbinates during nasal

surgery

2. Occurs following irradiation

3. Granulomatous infections like leprosy, syphilis, tuberculosis etc.

Pathology:

1. Metaplasia of ciliated columnar nasal epithelium into squamous

epithelium.

2. There is a decrease in the number and size of compound alveolar

glands

3. Dilated capillaries are also seen

Brain abscess pathology:

Stages of formation of brain abscess:

Stage of cerebral oedema: This is in fact the first stage of brain abscess

formation. It starts with an area of cerebral oedema and encephalitis. This

oedema increases in size with spreading encephalitis.

Formation of capsule: Brain attempts to wall off the infected area with theformation of fibrous capsule. This formation of fibrous tissue is dependent on

microglial and blood vessel mesodermal response to the inflammatory process.

This stage is highly variable. Normally it takes 2 to 3 weeks for this process to

be completed.

Liquefaction necrosis: Infected brain within the capsule undergoes liquefactive

necrosis with eventual formation of pus. Accumulation of pus cause

enlargement of the abscess.

Stage of rupture: Enlargement of the abscess eventually leads to rupture of the

capsule containing the abscess and this material finds its way into the

cerebrospinal fluid as shown in the above diagram.

Cerebellar abscess which occupy the posterior fossa cause raised intra cranial

tension earlier than those above the tentorium. This rapidly raising intra cranial

pressure causes coning or impaction of the flocculus or brain stem into the

foramen magnum. Coning produces impending death. If the walling off process

(development of capsule) is slow, softening of brain around the developingabscess may allow spread of infection into relatively avascular white matter,


37/44

www.drtbalu.co.in

leading to the formation of secondary abscesses separate from the original or

connected to the original by a common stalk. This is how multilocular

abscesses are formed. Eventually the abscess may rupture into the ventricular

system or subarachnoid space, causing meningitis and death.

VI. Microbiology: Answer any threeHIV virus:

This lentivirus a member of retrovirus family causes

Immunodeficiency syndrome. Infection with HIV is caused by:

1. Blood transfusion2. Semen3. Transfer via body fluids4. Breast milk

HIV virus infects the vital cells of human immune system like the T

lymphocytes. Specifically it affects the CD4 population of T lymphocytes. On

entering the target cell the viral RNA genome is converted to double stranded

DNA by the reverse transcriptase enzyme present inside the virus. This viral


38/44

www.drtbalu.co.in

DNA is integrated into the host DNA by another substance coded by the virus

known as integrase. On infection two things are possible:

1. The virus may remain dormant (latent stage) allowing the cell to performits normal functions

2. The virus may begin to proliferate and start to infect other cellspromoting viral transmission

Stages of HIV infection:

Incubation period This asymptomatic phase could last anywhere between 4-6

weeks.

Second stage Causes acute symptoms like fever, lymphadenitis, pharyngitis,myalgia and malaise.

Stage of latency Asymptomatic phase could last anywhere between 2 weeks

to 20 years.

Final stage This is brought out by the presence of opportunistic infections

due to suppression of immunity.

Diagram showing HIV viron particle

Structure of HIV virus:

HIV virus is roughly spherical with a diameter of 120 nanometer. It is about 60

times smaller than that of red blood cell. It contains two copies of single

stranded RNA that codes for the 9 genes that are present in the virus. The


39/44

www.drtbalu.co.in

single-stranded RNA is tightly bound to nucleocapsid proteins, p7 and enzymes

needed for the development of the viron such as reverse

transcriptase, proteases, ribonuclease and integrase. A matrix composed of the

viral protein p17 surrounds the capsid ensuring the integrity of the viron

particle. This in turn is surrounded by the viral envelope that is composed of

two layers of fatty molecules known as phospholipids. These fatty molecules

are derived from the membrane of human cell. Embedded in the viral

envelope are proteins from host cell and about 70 copies of complex HIV viral

proteins.
http://en.wikipedia.org/wiki/Reverse_transcriptasehttp://en.wikipedia.org/wiki/Reverse_transcriptasehttp://en.wikipedia.org/wiki/Aspartyl_proteasehttp://en.wikipedia.org/wiki/Ribonucleasehttp://en.wikipedia.org/wiki/Integrasehttp://en.wikipedia.org/wiki/Integrasehttp://en.wikipedia.org/wiki/Ribonucleasehttp://en.wikipedia.org/wiki/Aspartyl_proteasehttp://en.wikipedia.org/wiki/Reverse_transcriptasehttp://en.wikipedia.org/wiki/Reverse_transcriptase


40/44

www.drtbalu.co.in

Figure showing HIV replication cycle


41/44

www.drtbalu.co.in

Immunoglobulin A:

This immunoglobulin plays an important role in mucosal immunity.

More amounts of IgA are secreted over the mucous membranes of

the body than anywhere else in the body. It has been estimated that

about 2-5 g of IgA gets secreted each day in GI tract alone. It exits in

two forms IgA1 and IgA2 forms. This immunoglobulin can exist in two

forms:

The classic IgA

Secretory IgA This form is commonly seen in mucous secretions,

tears, saliva, colostrum etc. This type of immunoglobin is resistant to

the degradation effects of proteolytic enzymes.

IgA on binding to the bacterial / viral antigen initiates the antibody

dependent cell mediated cytotoxicity.

IgA is a poor activator of complement system. It is also considered to

be a poor opsonizing agent.


42/44

www.drtbalu.co.in

Figure showing IgA.

1 H chain

2. L chain

3. J chain

4. Secretory component

Candida:

Candida is a type of yeast. Candida albicans is a diploid fungus. It

could cause opportunistic infections involving oral cavity and genital

in humans.

Candida infections are an important feature of opportunistic

infections in immune compromised individuals. In healthy individuals

candida albicans is present as commensal in the oral cavity and gut.

Candida infections occur in:


43/44

www.drtbalu.co.in

1. HIV infected / immunocompromised patients. In the oral cavity itcauses oral thrush.

2. Altered normal body flora Loss of normal bacterial flora due toexcessive use of antibiotics / steroids

3. Altered normal physiology Indwelling catheters / cardiacsurgeries

Candida albicans exist in two forms:

1. The Yeast form this form is the resting / commensal form2. Filamentous form this is the infecting form (multicellular)

Factors contributing to the virulence of candida albicans:

1. Presence of surface molecules that permit adherence of theorganism to other structures

2. Acid proteases and phospholipases that could disrupt the cellmembrane

3. Ability to exist in dimorphic formBetahemolytic streptococci:

These are spherical gram positive cocci, non- sporing measuring

about 0.5 1.2 m. This was first described by Billroth in 1874 from

patients with wound infections. Later came the Lancefield

classification based on M protein precipitin reactions. Lancefield

established the critical role played by M protein in disease causation.

In preantibiotic era streptococcal infections caused great morbidity

and mortality. With the advent of modern antibiotics the morbidity

and mortality levels due to this organism has come down a last.

Streptococcus cause suppurative and non suppurative disorders.The suppurative spectrum includes:

1. Pharyngitis/tonsillitis2. Impetigo3. Pneumonitis4. Necrotizing fasciitis5. Osteomyelitis6. Otitis media7. Sinusitis


44/44

8. Meningitis9. Brain abscessNon suppurative sequelae include:

1. Rheumatic heart disease2. Acute glomerular nephritis

The cell wall of this organism is very complex and chemically diverse.

The antigenic components of the cell wall contribute to its virulence. The

extracellular components responsible for the virulence of the organism include

invasins and exotoxins. The outer most capsule is made up of hyaluronic acid.This outer capsule is more or less similar to that of host cell. It is this feature

that helps the organism to escape from the immune mechanisms of the body.

Virulence factors:

1. Extracellular products & toxins2. Pyrogenic exotoxins3. Nucleases4. Other enzymes like neuraminidase etc.

mgr medical university ms ent basic sciences march 2009 question paper with solution

Documents