WO

Friday

8. Describe anatomy of the tongue and related mouth structures

Tongue
The tongue is a mass of striated muscle covered by mucosa, which manipulates ingested material during
mastication and swallowing. The muscle fibers are oriented in all directions, allowing a high level of mobility.
Connective tissue between the small fascicles of muscle is penetrated by the lamina propria, which makes
the mucous membrane strongly adherent to the muscular core. The lower surface of the tongue is smooth,
with typical lining mucosa. The dorsal surface is irregular, having hundreds of small protruding papillae of
various types on its anterior two-thirds and the massed lingual tonsils on the posterior third, or root of the
tongue. The papillary and tonsillar areas of the lingual surface are separated by a V-shaped groove called
the sulcus terminalis.

On its dorsal surface (a), the posterior third of the tongue has the lingual tonsils and the anterior portion has
numerous lingual papillae of four types. Pointed filiform papillae provide friction to help move food during
chewing. Ridge-like foliate papillae on the sides of the tongue are best developed in young
children. Fungiform papillae are scattered across the dorsal surface, and 8-12 large vallate papillae (b) are
present in a V-shaped line near the terminal sulcus. Taste buds are present on fungiform and foliate papillae
but are much more abundant on vallate papillae.
(c) Diagram of a single taste bud shows the gustatory (taste) cells, the supporting cells whose function is not
well understood, and the basal stem cells. Microvilli at the ends of the gustatory cells project through an
opening in the epithelium, the taste pore. Afferent sensory axons enter the basal end of taste buds and
synapse with the gustatory cells. In the stratified squamous epithelium of the tongue surface, taste buds
form as distinct clusters of cells recognizable histologically even at low magnification (d). At higher power the
taste pore may be visible, as well as the elongated nuclei of gustatory and supporting cells. (140X and 500X;
H&E)

Teeth
In the adult human there are normally 32 permanent teeth, arranged in two bilaterally symmetric arches in
the maxillary and mandibular bones. Each quadrant has eight teeth: two incisors, one canine, two premolars,
and three permanent molars. Twenty of the permanent teeth are preceded by primary teeth (deciduous or
milk teeth) that are shed; the others are permanent molars with no deciduous precursors. Each tooth has
a crown exposed above the gingiva, a constricted neck at the gum, and one or more roots that fit firmly into
bony sockets in the jaws called dental alveoli.
The crown is covered by very hard, acellular enamel and the roots by a bone-like tissue called cementum.
These two coverings meet at the neck of the tooth. The bulk of a tooth is composed of another calcified
material, dentin, which surrounds an internal pulp cavity. Dental pulp is highly vascular and well-innervated
and consists largely of loose, mesenchymal connective tissue with much ground substance,
thin collagen fibers, fibroblasts, and mesenchymal stem cells. The pulp cavity narrows in each root as
the root canal, which extends to an opening (apical foramen) at the tip of each root for the blood vessels,
lymphatics, and nerves of the pulp cavity. The periodontal ligaments are fibrous connective tissue bundles
of collagen fibers inserted into both the cementum and the alveolar bone.

All teeth are similar embryologically and histologically.

(a) The dentition of the permanent teeth is shown, as well as the approximate age at eruption for each tooth.
 (b) Diagram of a molar’s internal structure is similar to that of all teeth, with an enamel-covered crown, cementum-
covered roots anchoring the tooth to alveolar bone of the jaw, and a slightly constricted neck where
the enamel and cementum coverings meet at the gingiva. Most of the roots and neck consists of dentin. A pulp
cavity extends into the neck and is filled with well-vascularized, well-innervated mesenchymal connective tissue. Blood
vessels and nerves enter the tooth through apical foramina at the root tips. Periodontal ligaments hold the tooth to
bone of the jaw.

9. Describe the histological of the tongue and taste buds

Lingual papillae

(a) Section of the dorsal surface of tongue showing both filiform (FI) and fungiform papillae (F). Both types are elevations
of the connective tissue (CT) covered by stratified squamous epithelium (SSE), but the filiform type is pointed and heavily
keratinized while the fungiform type is mushroom-shaped, lightly keratinized, and has a few taste buds.
(b) Micrograph shows a single very large vallate papilla with two distinctive features: many taste buds (TB) around the
sides and several small salivary glands (GL) emptying into the cleft or moat formed by the elevated mucosa surrounding
the papilla. These glands continuously flush the cleft, renewing the fluid in contact with the taste buds. (Both X20; H&E)

The lingual papillae are elevations of the mucous membrane that assume various forms and functions. There
are four types:
 Filiform papillae are very numerous, have an elongated conical shape, and are heavily keratinized, which
gives their surface a gray or whitish appearance. They provide a rough surface that facilitates movement
of food during chewing.
 Fungiform papillae are much less numerous, lightly keratinized, and interspersed among the filiform
papillae. They are mushroom-shaped with well-vascularized and innervated cores of lamina propria.
 Foliate papillae consist of several parallel ridges on each side of the tongue, anterior to the sulcus
terminalis, but are rudimentary in humans, especially older individuals.
  Vallate (or circumvallate) papillae are the largest papillae, with diameters of 1-3 mm. Eight to twelve
vallate papillae are normally aligned just in front of the terminal sulcus. Ducts of several small,
serous salivary (von Ebner) glands empty into the deep, moatlike groove surrounding each vallate papilla.
This provides a continuous flow of fluid over the taste buds that are abundant on the sides of these papillae,
washing away food particles so that the taste buds can receive and process new gustatory stimuli. Secretions
from these and other minor salivary glands associated with taste buds contain a lipase that prevents the
formation of a hydrophobic film on these structures that would hinder gustation.

Taste buds are ovoid structures within the stratified epithelium on the tongue’s surface, which sample the
general chemical composition of ingested material. Approximately 250 taste buds are present on the lateral
surface of each vallate papilla, with many others present on fungiform and foliate (but not the keratinized
filiform) papillae. They are not restricted to papillae and are also widely scattered elsewhere on the dorsal
and lateral surfaces of the tongue, where they are also continuously flushed by numerous minor salivary
glands.
A taste bud has 50-100 cells, about half of which are elongated gustatory (taste) cells, which turn over with a
7- to 10-day life span. Other cells present are slender supportive cells, immature cells, and slowly dividing
basal stem cells that give rise to the other cell types. The base of each bud rests on the basal lamina and is
entered by afferent sensory axons that form synapses with the gustatory cells. At the apical ends of the
gustatory cells, microvilli project toward a 2-μm-wide opening in the structure called the taste pore.
Molecules (tastants) dissolved in saliva contact the microvilli through the pore and interact with cell surface
taste receptors.
Taste buds detect at least five broad categories of tastants: sodium ions (salty); hydrogen ions from acids
(sour); sugars and related compounds (sweet); alkaloids and certain toxins (bitter); and amino acids such as
glutamate and aspartate (umami; Jap. umami, savory). Salt and sour tastes are produced by ion channels,
and the other three taste categories are mediated by G-protein-coupled receptors. Receptor binding
produces depolarization of the gustatory cells, stimulating the sensory nerve fibers that transmit information
to the brain for processing. Conscious perception of tastes in food requires olfactory and other sensations in
addition to taste bud activity.

10. Describe anatomy and function of the pathways to taste centers of the brain.
Gustatory pathway
The nerves responsible for taste transmit information to the solitary nucleus in the medulla, which in turn
projects to three different brain areas: 
 Ventral posteromedial nucleus (VPM) of the thalamus, which projects to the basal portion of
the postcentral gyrus (conscious gustatory perception)
 Hypothalamus (emotional component of gustatory perception)
 Amygdala (emotional component of gustatory perception)
 The first neuron of the taste pathway is
located in the ganglia of the facial, vagus,
and glossopharyngeal nerves. The afferent
gustatory nerve fibers join to form the
nerve tract that projects to the nucleus of
the solitary tract.

Second-order neurons project from the

medulla oblongata in three distinct
branches. Projections to the hypothalamus
and amygdala transmit the emotional
component of taste perception. Projections
to the ventral posterior nucleus (VPM) of
the thalamus transmit to the gustatory
cortex at the foot of the postcentral gyrus
for conscious taste perception.

Other source:
There are classically four taste qualities—sweet, sour, bitter, and salty—and there are corresponding taste
receptor cells for each of these modalities. A fifth quality has been proposed, termed savory, which is best
associated with a meaty broth because a fifth class of taste receptor cell has been identified, umami
(Japanese, flavor). Whereas we may think our gustatory system’s primary function is to identify foods, this is
more a role of sights and smells. Rather, the system is exquisitely organized to identify nutrients or harmful
agents in what we ingest, in relation to particular physiological processes: sweet and savory are key to
maintaining proper energy stores, salty for electrolyte balance, bitter and sour for maintaining pH, and bitter
also for avoiding toxins.
Taste is mediated by three cranial nerves, through their innervation of oral
structures: facial (VII), glossopharyngeal (IX), and vagus (X). The glossopharyngeal and vagus nerves also
provide much of the afferent innervation of the gut, cardiovascular system, and lungs. This visceral afferent
innervation provides the central nervous system with information about the internal state of the body.

The Ascending Gustatory Pathway Projects to the Ipsilateral Insular Cortex

Taste receptor cells are clustered in the taste buds, located on the tongue and at various intraoral sites.
Chemicals from food, termed tastants, either bind to surface membrane receptors or pass directly through
membrane channels, depending on the particular chemical, to activate taste cells. Taste cells are innervated
by the distal branches of the primary afferent fibers in the facial, glossopharyngeal, and vagus nerves. These
afferent fibers have a pseudounipolar morphology, similar to that of the dorsal root ganglion neurons. In
contrast to the nerves of the skin and mucous membranes, where generally the terminal portion of the
afferent fiber is sensitive to stimulus energy, taste receptor cells are separate from the primary afferent
fibers. For taste, the role of the primary afferent fiber is to receive information from particular classes of
taste receptor cells and to transmit this sensory information to the central nervous system, encoded as
action potentials. For touch, the role of the primary afferent fiber is both to transduce stimulus energy into
action potentials and to transmit this information to the central nervous system.
The central branches of the afferent fibers, after entering the brain stem, collect into the solitary tract of the
dorsal medulla and terminate in the rostral portion of the solitary nucleus. Recall that the caudal solitary
nucleus is a viscerosensory nucleus, critically involved in regulating body functions and transmitting
information to the cortex for perception of visceral information as well as the emotional and behavioral
aspects of visceral sensations.
The axons of second-order neurons in the rostral solitary nucleus ascend ipsilaterally in the brain stem, in
the central tegmental tract, and terminate in the parvocellular division of the ventral posterior medial
nucleus. From the thalamus, third-order neurons project to the insular cortex and the
nearby operculum, where the primary gustatory cortical areas are located. This pathway is thought to
mediate the discriminative aspects of taste, which enable us to distinguish one quality from another. The
insular gustatory cortex projects to several brain structures for further processing of taste stimuli. Projections
to the orbitofrontal cortex, as well as the cingulate cortex and other insular areas, are thought to be
important for integration with olfactory information, for the awareness of flavors. In addition, these cortical
areas may be important for the behavioral and affective significance of tastes, such as the pleasure
experienced with a fine meal or the dissatisfaction after one poorly prepared. A component of the processing
of painful stimuli also involves the limbic system cortex, and pain in humans is not without emotional
significance.
Although taste and visceral afferent information are distinct modalities and have separate central pathways,
the two modalities interact. In fact, linking information about the taste of a food and its effect on body
functions upon ingestion is key to an individual’s survival. One of the most robust forms of learning,
called conditioned taste aversion, associates the taste of spoiled food with the nausea that it causes when
eaten. Another name for this behavior is bait shyness, referring to a method used by ranchers to discourage
predators from attacking their livestock. In this technique, ranchers contaminate livestock meat with an
emetic, such as lithium chloride, which causes nausea and vomiting after ingestion. After eating the bait, the
predator develops an aversion for the contaminated meat and will not attack the livestock. People can
experience a phenomenon related to conditioned taste aversion, in which they develop an intense aversion
to food they ate before becoming nauseated and vomiting, even if the food was not spoiled and the illness
resulted from an unrelated viral infection. Experimental studies in rats have shown that such interactions
between the gustatory and viscerosensory systems, leading to conditioned taste aversion, may occur in the
insular cortex.
 General organization of
the gustatory
system. A. Ascending
gustatory
pathway. B. Approximate
location of the gustatory
cortex in the insular
cortex. The frontal and
parietal opercular regions
have been removed to
show the insular
cortex. C. MRI showing
insular cortex and
approximate region of the
gustatory cortex in the
insular cortex.

11. Identify the causes and describe the pathophysiology of decreased taste activity
The majority of patients who present with taste dysfunction exhibit olfactory, not taste, loss. This is because
most flavors attributed to taste actually depend on retronasal stimulation of the olfactory receptors during
deglutition. As noted earlier, taste buds only mediate basic tastes such as sweet, sour, bitter, salty, and
umami. Significant impairment of whole-mouth gustatory function is rare outside of generalized metabolic
disturbances or systemic use of some medications, because taste bud regeneration occurs and peripheral
damage alone would require the involvement of multiple CN pathways. Taste function can be influenced by
age, diet, smoking behavior, use of medications, and other subject-related factors including (1) the release of
foul-tasting materials from the oral cavity from oral medical conditions (e.g., gingivitis, purulent sialadenitis)
or appliances; (2) transport problems of tastants to the taste buds (e.g., drying, infections, or inflammatory
conditions of the orolingual mucosa), (3) damage to the taste buds themselves (e.g., local trauma, invasive
carcinomas), (4) damage to the neural pathways innervating the taste buds (e.g., middle ear infections), (5)
damage to central structures (e.g., multiple sclerosis, tumor, epilepsy, stroke), and (6) systemic disturbances
of metabolism (e.g., diabetes, thyroid disease, medications). Unlike CN VII, CN IX is relatively protected along
its path, although iatrogenic interventions such as tonsillectomy, bronchoscopy, laryngoscopy, endotracheal
intubation, and radiation therapy can result in selective injury. CN VII damage commonly results from
mastoidectomy, tympanoplasty, and stapedectomy, in some cases inducing persistent metallic sensations.
Bell’s palsy is one of the most common causes of CN VII injury that results in taste disturbance. On rare
occasions, migraine is associated with a gustatory prodrome or aura, and in some cases tastants can trigger a
migraine attack. Interestingly, dysgeusia occurs in some cases of burning mouth syndrome (also
termed glossodynia or glossalgia), as does dry mouth and thirst. Burning mouth syndrome is likely associated
with dysfunction of the trigeminal nerve (CN V). Some of the etiologies suggested for this poorly understood
syndrome are amenable to treatment, including (1) nutritional deficiencies (e.g., iron, folic acid, B vitamins,
zinc), (2) diabetes mellitus (possibly predisposing to oral candidiasis), (3) denture allergy, (4) mechanical
irritation from dentures or oral devices, (5) repetitive movements of the mouth (e.g., tongue thrusting, teeth
grinding, jaw clenching), (6) tongue ischemia as a result of temporal arteritis, (7) periodontal disease, (8)
reflux esophagitis, and (9) geographic tongue.
Although both taste and smell can be adversely influenced by drugs, taste alterations are more common.
Indeed, over 250 medications have been reported to alter the ability to taste. Major offenders include
antineoplastic agents, antirheumatic drugs, antibiotics, and blood pressure medications. Terbinafine, a
commonly used antifungal, has been linked to taste disturbance lasting up to 3 years. In a recent controlled
trial, nearly two-thirds of individuals taking eszopiclone (Lunesta) experienced a bitter dysgeusia that was
stronger in women, systematically related to the time since drug administration, and positively correlated
with both blood and saliva levels of the drug. Intranasal use of nasal gels and sprays containing zinc, which
are common over-the-counter prophylactics for upper respiratory viral infections, has been implicated in loss
of smell function. Whether their efficacy in preventing such infections, which are the most common cause of
anosmia and hyposmia, outweighs their potential detriment to smell function requires study. Dysgeusia
occurs commonly in the context of drugs used to treat or minimize symptoms of cancer, with a weighted
prevalence from 56 to 76% depending on the type of cancer treatment. Attempts to prevent taste problems
from such drugs using prophylactic zinc sulfate or amifostine have proven to be minimally beneficial.
Although antiepileptic medications are occasionally used to treat smell or taste disturbances, the use
of topiramate has been reported to result in a reversible loss of an ability to detect and recognize tastes and
odors during treatment.
As with olfaction, a number of systemic disorders can affect taste. These include, but are not limited to,
chronic renal failure, end-stage liver disease, vitamin and mineral deficiencies, diabetes mellitus, and
hypothyroidism. In diabetes, there appears to be a progressive loss of taste beginning with glucose and then
extending to other sweeteners, salty stimuli, and then all stimuli. Psychiatric conditions can be associated
with chemosensory alterations (e.g., depression, schizophrenia, bulimia). A recent review of tactile,
gustatory, and olfactory hallucinations demonstrated that no one type of hallucinatory experience is
pathognomonic to any given diagnosis.
Pregnancy is a unique condition with regard to taste function. There appears to be an increase in dislike and
intensity of bitter tastes during the first trimester that may help to ensure that pregnant women avoid
poisons during a critical phase of fetal development. Similarly, a relative increase in the preference for salt
and bitter in the second and third trimesters may support the ingestion of much needed electrolytes to
expand fluid volume and support a varied diet.
LO
1. Cara diagnosis rhinosinusitis (EPOS), rhinitis (ARIA)

2. Kapan harus di refer ke specialist ENT

ENT Referral Guidelines Nose
Epistaxis
Recurrent nose bleeds are common in all age groups. Young children usually bleed from Little’s area on the
anterior septum, elderly patients from higher or further back in the nose.Common risk factors include nose
picking, high blood pressure and aspirin / NSAID / warfarin usage.
Treatment: First aid measures; apply ice and pressure on the anterior, soft part of the nose. Sit the patient
upright with the head forward to avoid swallowing blood. If a bleeding point is visible on the anterior
septum, consider cautery with silver nitrate sticks. Topical vasocontrictors  may be helpful. Petroleum jelly or
anti-staphylococcal ointment can be used in minor cases. For severe bleeding attempt packing with ribbon
gauze or nasal tampons and refer to ENT.
When to refer: Refer to the emergency ENT clinic if there is persistent or severe bleeding, or a suspected
clotting disorder.

Snoring And Obstructive Sleep Apnoea

The prevalence of snoring and obstructive sleep apnoea (OSA) is high and under-recognized. 24% of men and
14% of women are habitual snorers and 5% of men have OSA. In children, tonsil and adenoid hypertrophy is
the commonest cause of OSA and adenotonsillectomy frequently completely relieves the condition. OSA
causes multiple awakenings during sleep. This has a serious impact on wakefulness and intellectual capacity.
There is mounting evidence that OSA can cause significant cardiovascular disease.
Treatment:  Weight loss, cessation of smoking and reduction in alcohol intake should be encouraged. Try
simple solutions to avoid sleeping on the back. Treat any nasal obstruction and consider nasal dilator strips.
The treatment of OSA is nasal CPAP which is a service best provided in the context of a sleep disorder clinic.
When to refer: If the above simple measures have failed and snoring is the primary complaint refer to ENT. If
there is substantial obesity and OSA refer to a specialist sleep centre for initial assessment. Mouth breathing
and snoring in children rarely warrant surgery, however refer children with OSA to ENT.

Nasal Obstruction
Over a fifth of the population have nasal complaints, of whom two thirds report nasal obstruction. Nasal
blockage may be associated with a decrease in quality of life, loss of work productivity, sleep disorders and
occasionally eustachian tube dysfunction.
Causes: Rhinitis, septal deviation, nasal polyps, adenoid hypertrophy, alar collapse, foreign bodies and rarely
tumours of the sinonasal region
When to refer:
Rhinitis: Allergen avoidance, particularly of house dust mite is crucial in the treatment of chronic allergic
rhinitis. In addition a 3 month trial of a topical nasal steroid spray should be used. This may be combined with
a topical or systemic antihistamine. Failure to resolve warrants a routine ENT referral.
Septal deviation: If an obvious septal deviation exists then a routine ENT referral is appropriate.
Nasal polyps: A one month course of steroid nose drops may be more effective than sprays but they are
more difficult to instill properly. Short courses of oral steroids may also be effective. If there is no resolution
of symptoms or if there is gross polyposis then refer to a routine ENT clinic.
Foreign bodies: If a child presents with a unilateral nasal blockage or foul / bloody discharge, then a foreign
body should be suspected and a referral to the emergency ENT service is appropriate.
Sinonasal malignancy: This is extremely rare but if this diagnosis is entertained then an urgent referral to the
ENT clinic is appropriate. Suspicious symptoms are persistent facial swellings, loosening of teeth, proptosis,
parasthesia of the cheek and unexplained nosebleeds.

Sinusitis
Symptoms: Acute sinusitis: Acute facial pain following an URTI (maxillary/upper dentition, frontal or nasal
bridge pain). The pain is usually unilateral and associated with purulent rhinorrhoea and fever.
Chronic sinusitis: is associated with less pain and a purulent rhinorrhoea or post-nasal drip. It is often
accompanied by chronic rhinitis symptoms.
Treatment: In acute sinusitis, pain relief and decongestants (such as ephedrine or xylometazoline nasal
drops) may be sufficient. If an antibiotic is required, amoxycillin (or erythromycin) for 5 days is usually
adequate. If the patient fails to respond consider the possibility of anaerobic or beta-lactamase organisms.
Plain sinus x-rays have limited use in the routine management of rhinosinusitis.
When to refer: Refer to the emergency ENT clinic if there are any complications of acute sinusitis, especially
peri-orbital cellulitis/abscess, deterioration of vision, severe systemic illness, drowsiness or vomiting (? intra-
cerebral complications ).Refer if there has been a  failure to respond to medical treatment.
Refer chronic rhinosinusitis and recurrent acute sinusitis to the routine ENT clinic.

Fractured Nose
Symptoms: Traumatic injury to the nose resulting in peri-nasal swelling, black eyes and nasal tenderness.
Treatment: On initial presentation, examine the nose to exclude a septal haematoma (a cherry – red bilateral
tender swelling with blockage) or a deviated nasal septum. Review the patient in the practice in one week
when the swelling has subsided. X-rays are unnecessary unless there are concerns about other facial
fractures.
When to refer: Patients with an uncomplicated or undisplaced fractured nose or those unconcerned with
cosmesis do not require ENT follow-up. Refer a patient with a septal haematoma to the emergency ENT
clinic. Patients who are unhappy with the cosmesis of the nose should be referred to the emergency ENT
clinic at 7 days post injury as a manipulation is possible up to 14 days after trauma.
3. Komplikasi dari rhinosinusitis, Risk factor, clinical finding

4. Kenapa rhinosunisitis harus cepet-cepet di refer ke THT

5. Kenapa dikasus dikasih anti-histamine generasi ke 2

6. Klasifikasi rhinosinusitis
7. Treatment rhinosinusitis