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Dr. T Balasubramanian
MS (ENT) Applied Basic Sciences
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.
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
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.
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
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.
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.
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.
Figure showing the relationship between recurrent laryngeal nerve and Berry’s ligament
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
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
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.
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
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.
Figure showing the nasal tip support structure
Figure showing the nasal tip tripod as viewed from below
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
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:
Facial nerve nucleus
Superior olivary complex
Contralateral reflex pathway:
Superior olivary complex decussation
Contralateral 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. 2. 3. 4. 5. 6.
Ossicular chain pathology Vestibular schwanomma Cochlear / retrocochlear deafness Brain stem lesions (multiple sclerosis, haemorrhage) Diseases involving facial nerve Diseases involving stapedius muscle (myasthenia gravis)
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. 2. 3. 4. 5. It is an objective test Non invasive Assess middle ear function accurately It is possible to test children 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
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.
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.
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.
Coordination of oral motor mechanism is very essential for generating complex speech sounds. This takes place at the level of cerebral motor cortex. Respiration: Respiration before phonation is slightly different from that of normal breathing. Inspiration is somewhat quicker and expiration is slightly slowed. Vocal fold vibrations: These vocal folds open and close allowing air from subglottic area to escape in a phased manner. The rate of vibration of vocal folds produces sound. The frequency of these vibrations is highly individualistic and is known as the fundamental frequency of the individual. The fundamental frequency can be adjusted by contraction of intrinsic muscles of larynx especially the thyroarytenoid which is known as the tuning fork of larynx. Positions assumed by vocal folds play a vital role in phonation. 1. When a sound like (f) is produced the vocal folds are held wide apart. 2. Sometimes during speech the vocal folds are completely closed and suddenly open to release air from subglottis due to increasing subglottic pressure levels. The sound thus generated is known as glottal stop. 3. Vibrations of vocal folds – this involves four stages. The first stage is closure / adduction where the vocal folds are brought together by contraction of laryngeal muscles. In the second stage the flow from the lungs still persists against the closed glottis causing an increase in subglottic pressure. This stage is known as compression. During the third stage the compressed air in the subglottic region would force the vocal folds to part and would escape. This is known as stage of release. During the fourth stage air flowing between vocal folds they are brought together due to the elasticity of vocal folds and the phenomenon known as Bernoulli’s effect. Bernoulli’s effect is development of negative pressure between the two vocal folds as air flows at a rapid pace between them. The glottis closes and the subglottic pressure rises again. This cycle keeps repeating during the act of phonation and is known as glottic cycle.
The loudness of voice is increased by increased contraction of abdominal muscles which increases the effective subglottic pressure causing an increase in the volume of sound generated. The average rate of glottic cycle in female is about 200 – 300 times / sec. In males the average rate of glottic cycle is about 150 times / sec. The rate of glottic cycle can be varied by individuals showing differences in pitch. Resonance: Resonance of sound produced is due to the presence of air in the nasal cavity, nasopharynx and sinuses. Resonances can be adjusted by changes in the position of tongue, jaws and lips. Articulators: These give life and meaning to the voice generated. The articulators include: 1. 2. 3. 4. 5. 6. 7. 8. Lips Jaw Teeth Different regions of tongue Gum ridge Hard palate Soft palate 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.
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.
Figure showing CSF circulation
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
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.
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)
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. 2. 3. 4. 5. Mucous – serves as lubricant Amylase – helps in digestion of starch Lingual lipase – Begins digestion of fat Electrolytes – Sodium chloride, potassium and bicarbonate 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.
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.
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.
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
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
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.
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
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
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. 2. 3. 4. 5. 6. 7. Weakness Visual disturbances Sweating Nausea Low blood pressure Slow heart rate 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
Treatment: 1. 2. 3. 4. Avoiding provoking stimuli Increase consumption of salt and fluids Voluntary tightening of leg muscles by crossing / uncrossing legs 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:
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,
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.
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
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
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.
Figure showing HIV replication cycle
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.
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:
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
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. 2. 3. 4. Extracellular products & toxins Pyrogenic exotoxins Nucleases Other enzymes like neuraminidase etc.