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Flashcards in Head and Neck Deck (56)
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Salivary glands

Salivary glands have secretory end pieces, the acini

About 1.5 litres of saliva is secreted daily.
pH of saliva varies from 7–8.


Content of saliva

1) Alpha-amylase and lipase (mostly from the lingual glands)
2) Mucins (glycoproteins) for lubrication and mucosa protection.

Saliva also contains bacteriostatic agents such as IgA, lysozyme and lactoferrin as well as proline-rich proteins which protect tooth enamel.


Electrolyte balance of saliva

Saliva is initially isotonic, with concentrations of Na, K, Cl and HCO3 close to those in plasma.

As this passes through the duct system the duct cells remove Na+ and Cl- in exchange for K+ and HCO3- and therefore becomes hypotonic.

Saliva in oral cavity is therefore:
A) Hypotonic
B) Alkaline
C) Rich in K+


Parotid, sublingual, submandibular acini secretion

The acini of the
1) Parotid is serous
2) Sublingual is mucous
3) Submandibular is mixed


Saliva secretion

1) Salivary secretion is under neural control.

2) Parasympathetic nerves stimulation (acetylcholine) increases secretion of watery saliva low in enzymic contents.

3) Also produces vasodilation through VIP

4) Atropine and other cholinergic antagonists reduce salivary secretion.

5) Food in the mouth and stimulation of vagal afferents increase secretion.


Function of saliva

1) It keeps the mouth moist, facilitates swallowing, stimulates taste buds and aids speech.

2) It has a bacteriocidal function.

3) Reduced salivary secretion = Dental caries.

4) Buffering action and neutralises any acid regurgitation on the oesophageal mucosa.


Phonation and larynx

Phonation is via adduction of the vocal cords. This involves the transverse arytenoid muscle and the recurrent laryngeal nerve.

Adduction of the vocal cords raises the subglottic pressure. When the air is exhaled it pushes the cords apart. The consequent drop in infraglottic pressure adducts the cords again and the cycle is repeated. The movements of the tensed cords will produce sound.

There are three important variables in sound:

• loudness
• pitch
• quality of sound



This varies with the level of infraglottic pressure needed to separate the cords and the degree of adduction of the cords.

Loudness is increased by tightly adducting the cords and building a higher infraglottic pressure.

The latter can be increased further by the contraction of expiratory muscles (as in shouting).


Pitch determined by?

This is determined by the frequency of vibration. Higher pitch is achieved by increasing the tension of the cord.


Muscle tone across the vocal cord for pitch

The cricothyroid muscle STRETCHES the cord by reducing the cricothyroid interval.

Simultaneous isometric contraction of the thyroarytenoid muscle increases the muscle tone contributing to an increase in the tension of the cord.


Quality of sound

The size and relationship of the resonating chambers such as the larynx, the pharynx and the paranasal sinuses contribute and maintain the quality of sound.

People with a good quality voice are born with it. They cannot be trained to produce it.


Articulation of sounds

1) Achieved by varying the size and shape of the oral cavity as well as interrupting the flow of exhaled air by lips, tongue, and palate.

2) Speech sounds are classified according to the structures used in modification of the expired jet of air.

3) The vowels are produced by altering the shape of the oral cavity by adjusting the jaws, cheek, tongue, and palate.

4) Consonants are produced by exhalation through the mouth, isolating the nasal cavity by raising the soft palate. By blocking the exhaled air by lips labial consonants such as P and B are articulated whereas T and D which are lingual consonants need approximation of the tongue against the palate. In nasal sounds such as M and N the soft palate is relaxed and air passes through both the nasal cavity and the oral cavity.


Articulation of sounds: Speech abnormality

1) Abnormalities in any structures involved in articulation can produce a speech defect.

2) In cleft palate, air always enters the nasal cavity giving nasal quality for the voice and affecting sounds which require contact between tongue and palate.

3) In unilateral paralysis of the recurrent laryngeal nerve the vocal cord on the paralysed side is in the cadaveric position and cannot be adducted. It will be at a lower level compared to the normal side.

4) Aphonia results at the onset of paralysis. Within a few days the opposite cord will cross the midline on phonation and approximate itself to the paralysed cord and the voice will return. However complete apposition of the two cords is impossible especially posteriorly. The voice will be harsh and low and it will never return to its normal quality.

5) Bilateral recurrent laryngeal nerve paralysis results in aphonia due to inability to adduct the vocal cords.

6) External laryngeal nerve paralysis which rarely happens in thyroid surgery paralyses the cricothyroid muscle resulting in inability to produce certain high- pitched sounds.


Articulation of sounds: CNS abnormalities

1) Disturbances in coordination of motor pathways as in cortical damages and extrapyramidal lesions pro- duce dysarthria.

2) In Parkinsons disease the tremor and muscular rigidity affect the muscles involved in speech causing rapid and monotonous speech with slurring of consonants and repetition of syllables.

3) Slurred speech is also characteristic of cerbellar lesions. Dysphasia results from lesions in the sensory cortex and some of the associated areas connected with speech.

4) The speech in these patients sounds normal but makes little sense. They are unable to comprehend what was heard or seen and hence produce inappropriate responses and often are unable to find appro- priate words or formulate sentences.

5) Such patients are capable of initiating speech but are unable to converse. Problems affecting the lower region of the primary sensory cortex (Warnicke’s area) and auditory association area will produce dysphasia.


Visual pathways

Impulses produced in the rods and cones in the retina by light reaches the visual cortex through the visual pathway. The visual pathway consists of:

• optic nerve
• optic chiasma
• optic tract
• lateral geniculate body
• optic radiation
• visual cortex


Optic nerve anatomy

1) The optic nerve commences at the lamina cribrosa, where the axons of the ganglion cells of the retina pierce the sclera.

2) The nerve fibres, about 1–1.2 million of them, acquire a myelin sheath at this point.

3) The optic nerve is covered by the dura, arachnoid and pia runs postero-medially in the orbit to enter the optic canal.

4) The nerve which is longer than the distance it has to transverse lies loosely in the orbital fat surrounded by the four recti muscles.

5) The ophthalmic artery accompanies the nerve. The artery which is superolateral to the nerve posteriorly crosses above the nerve to its medial side. It gives off the central artery of the retina which sinks into its inferomedial aspect.

6) In the optic canal the ophthalmic artery lies superolateral to the optic nerve. More proximally the nerve has a short course in the middle cranial fossa before uniting with the nerve of the opposite side at the chiasma.


Optic chiasma

See diagram

1) At the chiasma nerve fibres from the temporal half of the retina lie laterally and those from the medial half lie in the middle.

2) The middle fibres decussate. All the fibres that arise from the ganglion cells medial to a line passing through the fovea centralis cross from the optic nerve of that side to the optic tract of the opposite side.

3) The left optic tract thus contains fibres from the temporal half of the left retina and nasal half of the right retina.

4) As the temporal half of the retina perceives light from the nasal half of the visual field and the nasal half of the retina from the temporal visual field, the left optic tract transmits data from the right half of the visual field (and the right tract from the left half of the visual field).


Sella turcica and diaphragma sellae

Inferior to the optic chiasma lies the sella turcica containing the pituitary gland. The diaphragma sellae separates the pituitary gland from the optic chiasma. A tumour of the hypophysis cerberi may bulge the diaphragma sellae or break through it and press on the optic chiasma. The internal carotid artery lies lateral to the chiasma. Aneurysm of the artery at this level will compress the lateral fibres in the chiasma.


Optic tract

The optic tract passes postero-laterally from the chiasma. The tract forms the anterolateral boundary of the interpenduncular fossa crossing the cerebral peduncle to terminate in the lateral genicualte body.

Not all fibres of the optic tract end in the lateral geniculate body. Some enter the midbrain ending in the superior colliculus or the pretectal nucleus.

These fibres form the afferent limb of the light reflex.


Lateral geniculate body and optic radiation

The great majority of the fibres in the optic tract end in the lateral geniculate body. The six-layered lateral geniculate body has point-to-point representation at the retina. From the lateral geniculate body fibres of the optic radiation sweep laterally and backwards to the visual cortex in the occipital lobe.


Visual cortex

The visual cortex lies above and below the calcalcarine sulcus as well as on the walls of the sulcus. There is a point-to-point representation of the retina in the visual cortex. The upper half of the retina is represented on the upper lip of the calcarine fissure and the lower half on the lower lip. The macular region has a greater cortical representation than the peripheral retina facilitating acuity of vision for the macular region.


Visual tract lesions

Lesions of the retina or optic nerve result in uni- lateral blindness of the affected segment. Lesions of the optic tract and optic radiations produce controlateral homonymous hemianopia. Lesions of the middle fibres of the optic chiasma, as caused by a pituitary tumour, will cause bitemporal hemianopia.



1) Alternate phases of condensation and rarefaction of molecules produce sound waves. The loudness of the sound is proportional to the amplitude of the wave and its pitch is correlated with the frequency.

2) The ear converts sound waves in the air to action potentials in the auditory (cochlear) nerves. The waves are transmitted by the tympanic membrane (ear drum) through the movements of the auditory ossicles into the internal ear.

3) These produce movements in the fluid in the internal ear which in turn produce waves of movement of hair cells of the organ of Corti which generate action potentials in the nerve fibres.

4) Liquid is more difficult to move than air. The sound pressure in the air as it passes through the middle ear must, therefore, be amplified. Because the tympanic membrane is so much larger than the oval window the pressure (force per unit area) is increased 15–20 times when transmitted from the larger membrane to the smaller. The lever action of the ossicles also accentuates the pressure.

5) The auricle collects the sound waves and they pass along the external auditory meatus to produce vibra- tions of the tympanic membrane. The tympanic membrane is most efficient when the pressure on either side of it is equal. This is achieved by opening of the auditory tube which equalises the middle ear air pressure to that of the external auditory meatus.

6) The vibrations of the tympanic membrane are transmitted to the malleus, incus, and stapes. The malleus rocks on an axis through its long and short processes. When the handle of the malleus moves medially with the tympanic membrane, the head of the malleus and the body of the incus move laterally. As the body of the incus moves laterally its long


Tympanic reflex

When the middle ear muscles – the tensor tympani and stapedius contract they pull the malleus inwards and the stapes outwards, thus decreasing sound transmission.

Loud sounds initiate a reflex contraction of these muscles known as the tympanic reflex. It prevents strong sound waves from causing excessive stimulation of the hair cells and thus protects them from being damaged.


Conductive deafness

Conductive deafness results from failure of the conductive mechanism to transmit sound waves from the external ear to the inner ear. This can be due to various diseases of the external ear and middle ear. Sensory neuronal deafness is due to diseases of the organ of Corti, cochlea or the auditory nerve or its central pathway.


Physiology of smell

1) The olfactory receptors are located in the olfactory mucosa in the roof and upper part of the lateral wall and nasal septum.


Olfactory mucus

The olfactory mucus, produced by the Bowman’s glands in the olfactory mucosa may contain odour-binding proteins which will facilitate the passage of lipophylic odour producing substances through hydrophillic mucus. These proteins thus act as carrier proteins.



Most of the air passing through the nasal cavity will not come into contact with the olfactory mucosa. It passes mainly through the respiratory portion of the mucosa.

The turbinates warms the air and some of it rises by convection to come in contact with the olfac- tory region in and around the roof.

Sniffing, done by compression of the ala against the nose, helps to deflect the air upwards. It is a reflex response which occurs when a new or pleasant smell attracts attention.


Oral cavity:

Herpes simplex

Infections with the herpes simplex virus result in vesicles surrounded by a red margin appearing on the gingiva, cheek, lips or tongue. The vesicles break down to form shallow ulcers.

They may become encrusted and are frequently secondarily infected. These lesions are often very painful but heal spontaneously. The lesions are commonly associated with infections of the upper respiratory tract and pneumonia.

The virus may be in a dormant state in the squamous cells of many individuals and is activated by febrile illness. They also occur in the immunocompromised patient.


Oral cavity:


Oral candidiasis (thrush)
Seen in neonates and in immunocompromised patients such as those suffering from AIDS or those who are on immunosuppressant drugs and/or long term antibiotics is caused by the fungus Candida albicans. Lesions seen as white plaques in the mucous membrane, are con- fined to the epithelium and comprise of fungal hyphae, polymorphs and fibrin.