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The Tamilnadu Dr MGR Medical University MS (ENT)

Basic sciences
Question paper March 2009 with solutions

By

Dr. T Balasubramanian

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MS (ENT) Applied Basic Sciences

March 2009

I. Anatomy: Answer any four


Facial 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 nerve
Lateral – 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 ear
2. Used to place cochlear implant electrode into the cochlea via the
round window.
3. Horizontal portion of facial nerve can be accessed via this
approach. Hence this approach can be used to perform
decompression of horizontal division of facial nerve.

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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

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2. Fossa incudes superiorly
3. Chorda tympani laterally
4. Tympanic membrane anteriorly and laterally.

Trautman’s 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 dural
abscess 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.

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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
the recurrent 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

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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 nerve
does 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 a non recurrent variation of the right recurrent laryngeal
nerve. This condition places the nerve at risk during thyroid surgery.

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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 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. 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% of
patients it may lie anterior to the artery, and in 20% of cases it may lie deep to
the 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 recurrent
laryngeal nerve before entering the larynx.

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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's
ligament. The recurrent laryngeal nerve often passes through this layer to
enter the larynx.

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Figure showing the relationship between recurrent laryngeal nerve and
Berry’s ligament

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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 be
classified 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

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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

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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 sinus
drains 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 endoscopic
sinus surgery.
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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 quadrangular


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

Tardy’s classification of nasal tip support systems:

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

Tardy’s major support mechanisms include:

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

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

Tardy’s Minor tip support system includes:

1. Ligamentous sling spanning the domes of alar cartilages


2. Dorsal portion of cartilaginous nasal septum
3. Sesamoid complex extending the support of lateral crura to the pyriform
aperture
4. Attachment of alar cartilage to the overlying skin and musculature
5. Nasal spine
6. 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.

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Figure showing the nasal tip support structure

Figure showing the nasal tip tripod as viewed from below

II. Physiology: Answer any four


Stapedial 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

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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 tympanic
membrane impedance.

Ipsilateral reflex pathway:

Ipsilateral ear

Stapedius cochlear
Muscle nerve

Cochlear
Facial nerve
nucleus

Superior
Facial nerve
olivary
nucleus
complex

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Contralateral reflex pathway:

Contralateral
ear

Superior olivary
Stapedius
complex
Muscle
decussation

Contralateral
Facial nerve superior olivary
nucleus

Contralateral
facial nerve
nucleus

Uses of Stapedial reflex measurements:

1. It provides an objective measurement of patient’s hearing levels


2. Helps in identification of probable site of lesion in patients with
facial paralysis
3. Can identify malingerers

Complete absence of Stapedial reflex may be due to:

1. Ossicular chain pathology


2. Vestibular schwanomma
3. Cochlear / retrocochlear deafness
4. Brain stem lesions (multiple sclerosis, haemorrhage)
5. Diseases involving facial nerve
6. Diseases involving stapedius muscle (myasthenia gravis)

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7. To assess the pure tone threshold in a deaf mute child in order to
select 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 in


the 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 test
2. Non invasive
3. Assess middle ear function accurately
4. It is possible to test children
5. Malingering can easily be detected.

How to perform this test?

1. Patient should be alerted that loud sounds will he heard in either


ear. 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 should
be placed in the opposite ear.
3. Tympanometry is performed first. This is a must because acoustic
reflexes 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 unless
the patient has conductive deafness

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5. Tones are presented to the test ear at 0.5, 1, 2, and 4 kHz
frequencies 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 the
immitance probe will record it.
7. It should be ensured that the reflex is a true one and not an
artefact 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 the
basilar 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.

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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 of
auditory 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 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.

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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
3. Exercise
4. Hormones
5. Pregnancy
6. Fear / emotions
7. Sexual activity
8. 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 in
the nasal cycle.

The reason for nasal cycle still remains to be studied.

Mechanism of speech:

Speech process involves:


1. Speech centres in the brain
2. Respiratory centre in the brainstem
3. Respiratory system
4. Larynx
5. Pharynx
6. Nose / nasal cavities/sinuses
7. Structures of mouth and facial musculature

Speech centres in central nervous system:

Centres for speech recognition and production is situated on the left


hemisphere in 90% of right handed individuals, 60% of left handed individuals
and in 30% of ambidextrous individuals. Speech recognition and linguistic
expression are located in the Wernicke’s area of brain. This involves input
from visual and auditory areas. From this area stimuli are sent to Broca’s area
where vocalization control is located.

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Coordination of oral motor mechanism is very essential for generating complex
speech sounds. This takes place at the level of cerebral motor cortex.

Respiration:

Respiration before phonation is slightly different from that of normal


breathing. Inspiration is somewhat quicker and expiration is slightly slowed.

Vocal fold vibrations:

These vocal folds open and close allowing air from subglottic area to escape in
a phased manner. The rate of vibration of vocal folds produces sound. The
frequency of these vibrations is highly individualistic and is known as the
fundamental frequency of the individual. The fundamental frequency can be
adjusted by contraction of intrinsic muscles of larynx especially the
thyroarytenoid which is known as the tuning fork of larynx. Positions assumed
by vocal folds play a vital role in phonation.

1. When a sound like (f) is produced the vocal folds are held wide apart.
2. Sometimes during speech the vocal folds are completely closed and
suddenly open to release air from subglottis due to increasing subglottic
pressure levels. The sound thus generated is known as glottal stop.
3. Vibrations of vocal folds – this involves four stages. The first stage is
closure / adduction where the vocal folds are brought together by
contraction of laryngeal muscles. In the second stage the flow from the
lungs still persists against the closed glottis causing an increase in
subglottic pressure. This stage is known as compression. During the
third stage the compressed air in the subglottic region would force the
vocal folds to part and would escape. This is known as stage of release.
During the fourth stage air flowing between vocal folds they are brought
together due to the elasticity of vocal folds and the phenomenon known
as Bernoulli’s effect. Bernoulli’s effect is development of negative
pressure between the two vocal folds as air flows at a rapid pace
between them. The glottis closes and the subglottic pressure rises
again. This cycle keeps repeating during the act of phonation and is
known as glottic cycle.

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The loudness of voice is increased by increased contraction of abdominal
muscles which increases the effective subglottic pressure causing an increase
in the volume of sound generated.

The average rate of glottic cycle in female is about 200 – 300 times / sec.

In males the average rate of glottic cycle is about 150 times / sec. The rate of
glottic cycle can be varied by individuals showing differences in pitch.

Resonance:

Resonance of sound produced is due to the presence of air in the nasal cavity,
nasopharynx and sinuses. Resonances can be adjusted by changes in the
position of tongue, jaws and lips.

Articulators:

These give life and meaning to the voice generated. The articulators include:

1. Lips
2. Jaw
3. Teeth
4. Different regions of tongue
5. Gum ridge
6. Hard palate
7. Soft palate
8. Glottis

Importance of tongue as an articulator:


The tongue is the most mobile structure inside the oral cavity. It is
effectively composed of three articulators tip, blade and back of the
tongue. These areas of tongue by articulating with teeth, gum, hard
palate and soft palate generate various consonants. The jaw moves
upwards and downwards altering the size of the oral cavity thereby
providing the space necessary for tongue movements.

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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 absorbed
across 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 production
2. Arterial pulsations
3. Directional beating of ependymal cilia
CSF 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.

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Figure showing CSF circulation

III. Biochemistry: Answer any three


Endolymph 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 ATPase
2. Adenyl cyclase
3. Carbonic anhydrase

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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 can
lead 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.

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2. Shift of hydrogen ions into intracellular space: This invariably
develops 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 in
amounts 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 of
extracellular 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 perfusion


2. Stimulation of Renin angiotensin mechanism

Most common causes of metabolic alkalosis are:

1. Use of diuretics
2. External loss of gastric secretions

Types of metabolic alkalosis can be divided into:

Chloride responsive alkalosis (urine chloride <20mEq/L)

Chloride resistant alkalosis (urine chloride >20mEq/L)

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Causes of chloride responsive alkalosis (urine chloride <20mEq/L)

1. Loss of gastric secretions


2. Ingestion of large doses of non-absorbable antacids
3. Use of loop diuretics

Causes of Chloride resistant alkalosis with hypertension

1. Hyperaldosteronism
2. Liddle syndrome
3. Mutations involving mineralocorticoid receptors

Causes of chloride resistant alkalosis with normo-tension/hypotension

1. Bartter syndrome
2. Gitelman syndrome

Biochemical analysis of saliva:

Saliva contains 4 major components.

These are:

1. Mucous – serves as lubricant


2. Amylase – helps in digestion of starch
3. Lingual lipase – Begins digestion of fat
4. Electrolytes – Sodium chloride, potassium and bicarbonate
5. Proteins – Lysozymes, Histatins, cytatins and salivary peroxidase

Saliva is hypotonic to plasma. Sodium and chloride present in saliva are lower
in concentration when compared to that of plasma. Potassium and
bicarbonate levels are higher than that of plasma. Concentration of
electrolytes depends on salivary flow rates.

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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 /diphtheria
2. Atrophic rhinitis – Crusts are greenish and foul smelling
3. Extensive surgeries involving nasal mucosa
4. Gross deviations of nasal septum causing directional changes in
the nasal airway causing drying and crusting of nasal mucosa.
5. Exposure to toxins like chromium
6. Wegener’s 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 transformed
into keratinized squamous epithelium.

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

IV. Pharmacology: Answer any three


Aminoglycosides:
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.

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Drugs belonging to this group are active against a wide variety of
gram positive and negative bacteria.
Examples of drugs belonging to this group:
Streptomycin
Gentamycin
Neomycin
Tobramycin

Drugs belonging to this group are not reliably absorbed from the gut
and hence it should be administered parentally for optimal effect.

Toxicity:

1. Drugs belonging to this group are ototoxic


2. Nephrotoxic
3. Neurotoxic in high doses

These drugs are used to treat predominantly gram negative


infections.

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 nitrate
2. Copper sulphate
3. Tricholoroacetic acid
4. Cantheridin

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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 Cushing’s
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 anaesthesia
2. Infiltrative anaesthesia

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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 ½
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 three


Pathology 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 cavernous
sinus 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

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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 fibroblastic
varieties; 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. This
leads to a variety of hemodynamic responses which include:
1. Inhibition of cardiac muscle – This leads to negative chronotrophic
effect 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 to
a gross reduction in the blood pressure of the individual causing

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unconsciousness. The heart rate could be normal in these
patients.
3. Majority of people could have a mixture of both cardiac and
vascular phases of depression.

Signs & symptoms:

1. Weakness
2. Visual disturbances
3. Sweating
4. Nausea
5. Low blood pressure
6. Slow heart rate
7. Fainting

Triggers of vasovagal attacks:

1. Prolonged standing / upright sitting


2. Standing up very quickly
3. Stress
4. Painful unpleasant stimuli
5. Sudden emotional disturbances
6. Abdominal straining
7. Hyperthermia
8. Pressing down on throat / eyes etc.
9. High altitude
10. Drug induces

Tests for diagnosis of vasovagal attacks:

Tilt table test

Holter monitoring

Electrophysiolic studies

Echocardiogram

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Treatment:

1. Avoiding provoking stimuli


2. Increase consumption of salt and fluids
3. Voluntary tightening of leg muscles by crossing / uncrossing legs
4. 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:

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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 the
formation 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 developing
abscess may allow spread of infection into relatively avascular white matter,
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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 three


HIV virus:
This lentivirus a member of retrovirus family causes
Immunodeficiency syndrome. Infection with HIV is caused by:
1. Blood transfusion
2. Semen
3. Transfer via body fluids
4. 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

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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 perform
its normal functions
2. The virus may begin to proliferate and start to infect other cells
promoting 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

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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.

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Figure showing HIV replication cycle

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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.

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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:

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1. HIV infected / immunocompromised patients. In the oral cavity it
causes oral thrush.
2. Altered normal body flora – Loss of normal bacterial flora due to
excessive use of antibiotics / steroids
3. Altered normal physiology – Indwelling catheters / cardiac
surgeries
Candida albicans exist in two forms:
1. The Yeast form – this form is the resting / commensal form
2. 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 the


organism to other structures
2. Acid proteases and phospholipases that could disrupt the cell
membrane
3. Ability to exist in dimorphic form

Betahemolytic streptococci:
These are spherical gram positive cocci, non- sporing measuring
about 0.5 – 1.2 µm. 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/tonsillitis
2. Impetigo
3. Pneumonitis
4. Necrotizing fasciitis
5. Osteomyelitis
6. Otitis media
7. Sinusitis

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8. Meningitis
9. Brain abscess

Non suppurative sequelae include:

1. Rheumatic heart disease


2. 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 & toxins


2. Pyrogenic exotoxins
3. Nucleases
4. Other enzymes like neuraminidase etc.

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