A 52-year-old man presented with complaints of reduced sense of smell for 1 week along with a history of bad breath and nasal congestion/discharge for 2 years. On examination, dried nasal discharge was observed. The patient's symptoms are likely related to chronic rhinosinusitis, as obstruction of sinus drainage pathways can cause recurrent sinus infections leading to reduced sense of smell, nasal congestion, discharge, headache and bad breath. Chronic inflammation may have damaged the nasal mucosa, impairing its cleansing function and predisposing the patient to recurrent infections characterized by thick, foul-smelling discharge. Further evaluation and treatment are needed to confirm the diagnosis and properly manage the patient's condition.

1. Medical Faculty Makassar, 3rd October 2017
Muslim University Of Indonesia
PBL REPORT
“SMELLING”
SPECIAL SENSE MODULE
WRITTEN BY:
GROUP 14
11020150009 Aulia Amani
11020150024 Nada Nahda
11020150033 Ainun Jariah Muliadi
11020150059 Nur Zamzam Azizah
11020150065 Afrilia Chaerunnisa
11020150081 A. ST. Zuraidha P.A
11020150089 Indah Chintya Maharani
11020150096 Muhammad Rizky Hidayat
11020150109 Reza Novriadi Khautsari
11020150119 Asyaratun Qamila
Tutor :
dr.Abdul Mubdi
MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
2016

2. SCENARIO 2
A 52-year-old man came to THT with a complaints of reduced inhabitants experienced
since 1 week ago. Previously patients often complained of his bad breath smelling. History
of pain at the base of the nose, often headache accompanied by greenish yellow-thick snot
since 2 years ago. On examination of the nose found piles of dried snot.
I. DIFFICULT WORD
-
II. KEY WORD
- A 52-year-old man
- Complaints of reduced inhabitants experienced since 1 week ago
- Bad breath smelling
- pain at the base of the nose
- headache
- greenish yellow-thick snot since 2 years ago
- piles of dried snot
III. QUESTIONS
1. How does the olfactory track occurs ?
2. What are the etiology of hyposmia ?
3. What are the diseased can cause hyposmia ?
4. What caused the patient have runny nose ?
5. Why the color of mucouse is yellow and greenish ?
6. Why the patient have smells bad breath ?
7. Why do the patient get headache?
8. Relation of the each symtoms ?
9. How to diagnosed the patient ?
10. Diffrential Diagnosis?
11. Therapy and first treatment to the patient ?

3. IV. ANSWER
1. How does the olfactory tract occurs?
Anatomy and Physiology Olfactory system1,2
The olfactory neuroepithelium is located at the upper area of each nasal chamber
adjacent to the cribriform plate, superior nasal septum, and superior-lateral nasal wall. It
is a specialized pseudostratified neuroepithelium containing the primary olfactory
receptors. In neonates, this area is a dense neural sheet, but, in children and adults, the
respiratory and olfactory tissues interdigitate. As humans age, the number of olfactory
neurons steadily decreases. In addition to the olfactory neurons, the epithelium is
composed of supporting cells, Bowman glands and ducts unique to the olfactory
epithelium, and basal cells that allow for the regeneration of the epithelium.
The sense of smell is mediated through stimulation of the olfactory receptor cells by
volatile chemicals. To stimulate the olfactory receptors, airborne molecules must pass
through the nasal cavity with relatively turbulent air currents and contact the receptors.
Odorants can also be perceived by entering the nose posteriorly through the nasopharynx
to reach the olfactory receptor via retronasal olfaction. This mechanism is thought to play
a key role in the sensation of flavor during eating and drinking. Odorants diffuse into the
mucous and are transported to the olfactory receptor with the help of odorant-binding
proteins. Important determinants of an odor's stimulating effectiveness include duration,
volume, and velocity of a sniff.
Each olfactory receptor cell is a primary sensory bipolar neuron. The average nasal
cavity contains more than 100 million such neurons. The olfactory neurons are unique
because they are generated throughout life by the underlying basal cells. New receptor
cells are generated approximately every 30-60 days.

4. Each regenerating receptor cell extends its axon (CN I) into the CNS as a first-order
olfactory neuron and forms synapses with target mitral and tufted cells in the olfactory
bulb.
The bipolar olfactory neurons have a short peripheral process and a long central
process. The peripheral process extends to the mucosal surface to end in an olfactory knob,
which has several immobile cilia forming a dense mat at the mucosal surface. The cilia
express the olfactory receptors that interact with odorants. The family of odor receptor
proteins are G-protein coupled receptors (GPCRs) associated with adenylate cyclase. The
genes that encode them were discovered in 1991 by Linda Buck and Richard Axel,
culminating in the Nobel Prize awarded in 2004.
This family encompasses approximately 900 genes, the largest in the genome. It has
been found in mice that each neuron expresses only one gene, so odorants are recognized
by the complex binding pattern they create. This is most likely the case in humans as well.
Interestingly, these genes have been recently discovered to exist in nonolfactory tissues
such as sperm and the gut. The function of these genes outside of their role in olfaction is
under investigation.
Once an odorant binds to its receptor, a signaling cascade depolarizes the neuron,
which sends the signal along its axon, which then converges together within the bundled
axons of the fila olfactoria deep to the epithelium.
These axons project through the cribriform plate to the ipsilateral olfactory bulb. The
olfactory bulb cells contacted by the olfactory receptor cells include the mitral and tufted
cells, arranged in specialized areas termed glomeruli. The axon terminals of receptorlike
neurons synapse within the same glomeruli, forming an early topographical odorant map.
Therefore, an odor is thought to activate a set of odorant receptors based on its chemical
composition. The corresponding glomeruli of the olfactory bulbs are in turn activated,
creating a unique pattern of excitation in the olfactory bulb for each odorant.
The glomerular cells are the primary output neurons of the olfactory bulb. Axons from
these cells travel to the olfactory cortex, which is divided into 5 parts, including (1) the
anterior olfactory nucleus, connecting the 2 olfactory bulbs through the anterior

5. commissure, (2) the olfactory tubercle, (3) the pyriform cortex, which is the main olfactory
discrimination region, (4) the cortical nucleus of the amygdala, and (5) the entorhinal area,
which projects to the hippocampus.
The olfactory pathway does not involve a thalamic relay prior to its cortical
projections. Relays from the olfactory tubercle and the pyriform cortex project to other
olfactory cortical regions and to the medial dorsal nucleus of the thalamus and probably
involve the conscious perception of odors.
Conversely, the cortical nucleus of the amygdala and the entorhinal area are limbic
system components and may be involved in the affective, or hedonic, components of odors.
Regional cerebral blood flow (measured with positron emission tomography) is
significantly increased in the amygdala with introduction of a highly aversive odorant, and
it is associated with subjective ratings of perceived aversiveness.
The vomeronasal organ (VNO), or Jacobson organ, is a bilateral membranous structure
located within pits of the anterior nasal septum, deep to the nasal respiratory mucosa and
next to the septal perichondria. Its opening in the nasal vestibule is visible in 91-97% of
adult humans, and it is 2 cm from the nostril at the junction of the septal cartilage with the
bony septum. Unlike lower animals, axons projecting from the VNO have not been found
in postnatal humans.
The VNO is believed by some to detect external chemical signals termed pheromones
or vomeropherins through neuroendocrine-type cells found within the organ. These signals
are not detected as perceptible smells by the olfactory system and may mediate human
autonomic, psychologic, and endocrine responses.
Free trigeminal nerve endings, which are stimulated by aversive or pungent stimuli
(eg, ammonia), exist in the nasal mucosa. These are processed via separate pathways from
those in the olfactory system, described above.
2. What are the etiology of hyposmia ?
Hyposmia can be caused by obstruction of the nose, as in allergic rhinitis, vasomotor
rhinitis, atrophic rhinitis, konka hypertrophy, septal deviation, polyps, tumors. Can also
occur in some systemic diseases, such as diabetes, kidney failure and liver failure and the
use of drugs such as antihistamines, decongestants, antibiotics, antimetabolites, anti-
inflammatory and antithyroid. 2

6. 3. What are the diseased can cause hyposmia ?
The disead can cause hyposmia are :3,4
- Rhinitis: Inflammation or irritation that occurs dimembrane nasal mucosa.
- Konka hypertrophy: Enlarged nasal lymph nodes that function to catch germs and
control infections, often due to infections and chronic irritation, bias also due to
allergies.
- Septum deviation: Physical abnormalities of the nose that occur when a wall separating
two nostrils shifts away from the center, making one nasal passage smaller than the
other.
- Polyps: Mucous membranes that have hypertrophy or inflammation so that the size of
the cell enlarged.
- Tumors: The growth of abnormal body cells due to a malignancy that causes the
emergence of a mass.
- Trauma capitis: Injury or injury both physical and psychic caused by physical actions
with the breakdown of the normal continuity of a structure.
4. What caused the patients have rany nose?
The cause of rany nose in general is :5
1) Human rhinovirus (HRV) is the group of viruses that cause the most common colds.
In addition to the virus, this disease can also be caused by coronavirus, adenovirus,
human parainfluenza virus (HPIV), and respiratory syncytial virus (RSV).
2) Specific chronic infections by other germs
3) Deficiency of iron and vitamin A
4) Progress
5) Environment
6) Chronic sinusitis
7) Imbalance of estrogen hormone
8) Collagen disease that includes autoimmune disease
9) Hereditary
10) Suparanasi on the nose and paranasal sinuses
11) Blood type
The following factors may increase the risk of catching colds, behind:5
1) Being in a crowd of people (in markets, schools, offices, or public transport)
2) Have a low body system
3) Have a history of chronic diseases
4) Children Smoking
5) Cold air

7. 5. Why the color of mucouse is yellow and greenish ?
Patomekanism of the green-yellow and dry secret of the nose6,7
There are many things can cause the nasal secretions such a trauma, localized local
infection, further effects of surgery, radiation, and subsequent inflammation of the nose.
If this inflammation lasts long and does not heal, it is called chronic inflammation. This
chronic inflammation will cause many anatomic changes and nasal function. In this case,
it suspected caused by subsequents infections. The bacteria cause normal ciliary activity
in the human nasal mucosa stops. At first, the epithelial and ciliated epithelial cells that
are epithelial cells present on the nasal cones will be lost. This epithel undergoes initial
stratification and metaplasia (transformed into another adult cell, in which case the cilliated
stratifacted epithelium is transformed into a flat epithelium)
The ciliated epithelial epithelial metaplasia of the ciliated epithelial epithelium will
cause a lack of cleansing ability and the ability to clean debris (since this is a function of
cilia, so if the silica has been lost the cleaning ability and debris clearance also disappears),
Subsequent effects of mucosal glands may be atrophy and may even disappear, the
formation of extensive subepithelial tissue fibrosis, surfactant function will become
abnormal. Surfactant deficiency is a major cause of decreased nasal immunity to infection.
The abnormal surfactant function causes clench clucens, and has an adverse effect on
the frequency of cilia movement (nasal hair) that will make the mucus spill, the thinner the
epithelium (atrophy konkha) will make the nasal cavity widen, due to the drought, the
formation of crust, and mucosal irritation is widespread.
Then if bloodsupply is also inadequate, it will occur cell and tissue necrosis which
when later can the process of decomposition and mixed with toxins from microorganisms
will result in a foul-smelling greenish pus that dries up in call crusts. crust that is a very
good medium for growth of germs. If crust is released it will make epistaxis.
In addition to atrophy of the mucosa, it can also occur atrophy of the olfactoria mucosa
that can cause the patient to experience hyposmia or even anosmia (ability to smell).
6. Why patient have smelled bad breathe?
Nasal causes.8
Postnasal drip (caused by mucus of the paranasal sinuses) contacting the dorsum of the
tongue is largely involved. Foreign bodies in the nasal cavity can produce a foul odour as
well. Also a cleft palate can be the origin of bad breath. Atrophic rhinitis with bacterial
surinfection causes malodour too. This can be caused by tumor rescetions, radiotherapy or
overuse of decongestives or cocaine.
Sinusitis. 8
Bacterial sinusitis develops mostly out of acute viral sinusitis. Streptococcus
pneumonia and Haemophilus influenza are the main responsible bacteria. On radiological

8. or computed tomography (CT) images, fading is perceived. When purulent mucous is
produced, a typical odour appears. In 10% of the sinusitis cases, a tooth or several teeth
are involved. In these cases, the spotted bacteria are: Peptostre- tococcus spp.,
Fusobacterium spp., Prevotella spp. and Porphyromonas spp. Since those bacteria are able
to produce VSCs, a clear association to halitosis is available. The treatment of dentogenic
problems (even- tual with the additional use of antibiotics) decreases the anaerobic
pathogens, even as the odour problem. In the case of chronic sinusitis, 50%–70% of the
patients complain about oral malodour.
7. Why do the patient get headache?
a. Sinus headaches
Sinuses are air-filled spaces inside forehead, cheekbones, and behind the bridge of
your nose. When they get inflamed, usually because of an allergic reaction or an infection,
they swell, make more mucus, and the channels that drain then can get blocked. The build-
up of pressure in sinuses causes pain that feels like a headache.
Symptoms
Deep and constant pain in cheekbones, forehead, or the bridge of the nose. The
pain usually gets stronger when moving head suddenly or strain.
Other kinds of recurring headaches, like migraines or tension headaches are often
mistaken for sinus headaches. If a sinus blockage, such as infection, really is the cause, we
will likely have a fever.9
b. Migraine headache
Migraine was previously considered to be a vascular phenomenon that resulted
from intracranial vasoconstriction followed by rebound vasodilatation. Currently,
however, the neurovascular theory describes migraine as primarily a neurogenic process
with secondary changes in cerebral perfusion associated with a sterile neurogenic
inflammation.10
c. Tension Headache
Etiology:
- Stress and/or anxiety
- Poor posture
- Depression
Pathophysiology
Both muscular and psychogenic factors are believed to be associated with tension-
type headache. A study by Kiran et al indicated that patients with chronic tension
headaches for longer than five years tend to have lower cortisol levels. This was postulated
to be due to hippocampus atrophy resulting from chronic stress.11

9. 8. Relation of the each symtoms ?
Subjective symptoms are divided into systemic symptoms and local symptoms.
Systemic symptoms are fever and lethargy. Local symptoms of the nose are thick,
occasionally smelly and felt noses flowed into the nasopharynx. Feeling nasal congestion,
pain in the affected sinus area, and sometimes felt also elsewhere due to pain overpower
(referred pain).12
Pathophysiology rhinosinusitis is associated with 3 factors, namely (Brook, 2015):12
a. Obstruction of Sinus Drainage Path (Ostia Sinus)
Obstruction of sinus ostia prevents normal mucus drainage. Ostia can be blocked by
swollen mucosa or local causes (eg, trauma and rhinitis), as well as by certain systemic
inflammatory disorders associated and immune disorders. Systemic diseases resulting in
decreased mucociliary clearance, including cystic fibrosis, respiratory allergies, and
primary ciliary dyscinesia (Kartagener syndrome), may be a predisposing factor for acute
sinusitis in rare cases. Patients with immunodeficiency (eg, agammaglobulinemia,
combined with variable immunodeficiency, and immunodeficiency with decreased
immunoglobulin G [IgG] - and immunoglobulin A [IgA]) also increase the risk of
progression to acute sinusitis.
Mechanical obstruction due to nasal polyps, foreign bodies, septum deviation, or
tumors can also cause ostial blockage. In particular, the anatomical variations that narrow
the ostiomeatal complex, including septal deviation, paradoxical conjunctive media, and
Haller cells make this area more sensitive to obstruction due to mucosal inflammation.
Typically, edematous edema of the mucosa has a toothed appearance, but in severe cases,
the mucus can actually fill the sinuses making it difficult to distinguish the allergic process
from infectious sinusitis. Typically, all affected paranasal sinuses and adjacent nasal cones
have edema. Air-fluid levels and bone erosion are not a feature of simple allergic sinusitis.
However, a swollen mucosa in poor sinus drainage is more susceptible to secondary
bacterial infections.
b. Hypoxia in the blocked sinuses is thought to cause ciliary dysfunction and changes in
mucus production to impair the normal mechanisms for mucus clearance.
c. Changes in Quantity and Quality of Mucus
Synonym secretion plays an important role in the pathophysiology of rhinosinusitis.
Mucous coat that lines the paranasal sinus contains mucoglycoproteins, immunoglobulins,
and inflammatory cells. This layer consists of two parts: (1) the inner serous layer (ie, the
sol phase) when the cilia are not in the resting phase and (2) the outer layer, the thicker
layer (ie, gel phase), transported by the moving cilia. The right balance between the inner
sole phase and the outer gel phase is essential for normal mucociliary clearance.
If the mucus composition changes and the resulting mucus is more viscous (eg, as in
cystic fibrosis), transport to the ostia is much slowed down, and the gel layer proves to be
thicker. This results in a collection of thick mucus that is retained in the sinus for various

10. periods. In the presence of a lack of secretion or loss of moisture on surfaces that can not
be compensated by mucous glands or goblet cells, the mucus becomes more viscous and
the sol phase can become very thin allowing the gel phase to have intense contact with the
cilia and impede their movement. Excess mucus can overwhelm the mucociliary cleansing
system, resulting in the secretion retained in the sinuses.
d. In frontal sinusitis localized pain is felt on the forehead or felt pain throughout the
head. Pain in sfenoid sinusitis in the vertex, occipital, behind the eyeball, and in the
mastoid area
9. How to diagnosed the patient ?
The step to diagnose are :13,14
Anamnesis
1) Is there a nose blockage?
2) Is there a tenderness in the nasal basin or not?
3) Has your nose ever been injured?
4) Do you have any history of allergies?
5) Has there been a previous history of nasal disease?
6) Is there a seasonal change in your symptoms? If so, which season is the worst?
7) Have you ever had a doctoral medicine before?
8) Do you have other prior history of illness?
9) Was there a history of previous drug use?
 antihistamines,
 decongestants,
 antibiotics,
 antimetabolites,
 anti-inflammation
 antithyroid
10) Does your family or your nearest person have the same illness as you? If yes, how
often do you meet that person?
Physical examination
- Preliminary
Inward anterior and inferior nasal infiltration. Usually the gentle emphasis on the front
end of the patient's nose with your thumb will widen the nostril (nostril) and with the help
of a small penlight or otoscope light, you can see most of the vestibulum of each nose. ]
when the tip of the nose feels painful to the touch "do this action carefully and wherever
possible not manipulate the nose.Note any symmetry or deformity of the nose.

11. The obstruction test, if necessary, is done by pressing both nostrils alternately and
asking the patient to breathe. Tenderness on the tip of the nose or the nostril shows a local
infection such as furuncle.
- Inspection
Inspect the inside of the nasal cavity with the largest otoscope and ear speculum.
Ask the patient to tilt his head slightly back and carefully insert the speculum into the
vestibule of each nostril by avoiding touch with a sensitive rice septum. Hold the otoscope
handle on one side to avoid the chin of the patient and increase your mobility. By directing
the speculum to the posterior, then upward through some kecif steps try to see the inferior
cones and media, the rice septum, and the narrow nasal passages between the two
structures. Some asymmetrical conditions on both sides are normal.
Anterior rhinoscopic examination
Note:
11) Nasal mucosa covering the septum and konka nasalis. Pay attention to its color and
any baffle; bleeding or exudate. If there is exudate, consider its character: clear,
mucopurulent or purulent. Normally the nasal mucosa appears slightly redder than
the oral mucosa. In viral rhinitis, the nasal mucosa appears red and swollen in
allergic rhinitis, the mucosa may appear pale, bluish or red.
12) Septum rice (nasal cavity). Note any deviation, inflammation or perforation of the
rice septum. The anterior portion of the rice septum (which can be reached by the
patient's fingers) is an area that is often the source of epistaxis (nosebleed). Fresh
or crusting blood can be seen. Causes of perforation of the septal seperium include
trauma, surgery, and the use of cocaine or intranasal amphetamines.
13) Any abnormalitss such as ulcers or polyps. Polyps are pale and semitranslusen
masses that usually come from the media meatus. Ulcers can occur because of the
use of cocaine is inhaled through the nose.
Get used to put all the nasal or ear speculum that is used is outside your instrument
box. Then, discard the disposable speculum or if the speculum is still to be used again (eg

12. nondisposable metal speculum), wash and disinfect properly. (You should check the
policies issued by your hospital regarding this procedure).
- Palpation
Palpate to find pain in sinus. Press the frontal sinus area from the bottom of the
eyebrows by avoiding the emphasis on the eyeball. Then press the maxillary sinus area.
Localized tenderness that occurs along with other symptoms, such as pain, fever, and
runny nose suggests acute sinusitis involving the frontal and maxillary sinuses.
Transillumination xamination may be a useful diagnostic tool.
Palpation
Supporting examination
Transillumination is a simple examination primarily to assess the condition of the
maxillary sinus. Examination is considered meaningful when there is a difference in
transillumination between the right and left sinuses. However, transillumination is not a
substitute for radiography in the evaluation of sinus disease.
Nasal endoscopy can assess nasal cavity conditions, presence of secretions,
osteomeatal complex patency, conjunctive size, edema around the tubal orifice, adenoid
hypertrophy and sinus mucosa appearance. Nasal endoscopy is better in lighting than
anterior rhinoscopy for examination of the medius and superior meatus. An indication of
nasal endoscopy is evaluation when conservative treatment fails.
Radiology is a common adjunct, including X-photographs, CT-Scan, MRI and
ultrasound. CT-Scan is the preferred modality in assessing the sinus pathology and
anatomy process, as well as for the evaluation of advanced rhinosinusitis when medical
treatment does not respond. It is necessary in chronic rhinosinusitis to be performed
surgery. The primary preferred investigation to assess the sinus image is CT-scan. The
advantage is to be able to give a sinus image in chronic rhinosinusitis whose symptoms
are not appropriate with clinical examination. Diagnosis can be established with or without
naso-endoscopy. However, CT scans have limitations that are difficult to distinguish
rhinosinusitis from upper respiratory viral infections, unless complications arise. Optimal
visualization is obtained with coronal scans. Another investigation is a plain photograph,
ie with the position of Waters, PA and lateral. Usually the photo is only able to assess the

13. condition of large sinuses such as the maxillary and frontal sinuses. The sinuscopy is
performed by puncture through the medial wall of the maxillary sinus through the inferior
meatus and with the endoscopic tool can be seen the actual maxillary sinus condition.
Further action can be performed sinus irrigation for therapy. MRI is only performed if
there is suspicion of complications in orbital and intracranial.
Other examination that can be done include:
1. Nasal cytology, biopsy, aspiration puncture and bacteriology
2. Allergy testing
3. Mucociliary function tests: mucociliary cliren, cilium vibration frequency, electron
microscopy and nitric oxide
4. Assessment of nasal airflow: nasal inspiratory peakflow, rinomanometry, acoustic
rinometry and rinostereometry
5. The olfactory function test: threshold testing
6. Laboratory: CRP examination (C-reactive protein)
Waters Position
PA Position

14. Lateral Position
10. Diffrential Diagnosis?
a. Nasal polyp15,16
Definition
Nasal polyps are a soft, white or grayish mass present in the nasal cavity. Polyps
come from swollen nasal mucosa that contains a lot of interseluler fluid and then pushed
into the nasal cavity by gravity.
Nasal Polypi are non-neoplastic masses of oedematous nasal or sinus mucosa.
They are divided into two main varieties:
1) Bilateral ethmoidal polypi.
2) Antrochoanal polyp.
Bilateral Ethmoidal Polypi
Aetiology. Aetiology of nasal polypi is very complex and not well-understood.
They may arise in inflammarory conditions of nasal mucosa (rhinosinusitis), disorders of
ciliary motility or abnormal composition of nasal mucus (cystic fibrosis). Various diseases
associated with the formation of nasal polypi are:
1. Chronic rhinosinusitis. Polypi are seen in chronic rhinosinusitis of both allergic
and non-allergic origin. Non-allergic rhinitis with eosinophilia syndrome
(NARES) is a form of chronic rhinitis associated with polypi.
2. Asthma. 7% of the patients with asthma of atopic or non-atopic origin show nasal
polypi.
3. Aspirin intolerance. 36% of the patients with aspirin intolerance may show polypi.
Sampter's triad consists of nasal polypi, asthma and aspirin intolerance.
4. Cystic fibrosis. 20% of patients with cystic fibrosis form polypi. It is due to
abnormal mucus.
5. Allergic fungal sinusitis. Almost all cases of fungal sinusitis form nasal polypi.
6. Kartagener's syndrome. This consists of bronchiectasis sinusitis, situs inversus and
ciliary dyskinesis.

15. 7. Young's syndrome. It consists of sinopulmonary disease and azoospermia.
8. Churg-Strauss syndrome . Consists of asthma, fever, eosinophilia, vasculitis and
granuloma.
9. Nasal mastocytosis. It is a form of chronic rhinitis in which nasal mucosa is
infiltrated with mast cells but few eosinophils. Skin tests for allergy and IgE are
normal.
Pathogenesis.
Nasal mucosa, particularly in the region of middle meatus and turbinate becomes
oedematous due to collection of extracellular fluid causing polypoidal change. Polypi
which are sessile in the beginning become pedunculated due to gravity and the excessive
sneezing.
Pathology.
In early stages, surface of nasal polypi is covered by ciliated columnar epithelium
like that of normal nasal mucosa but later it undergoes a metaplastic change to transitional
and squamous type on exposure to atmospheric irritation. Submucosa shows large
intercellular spaces filled with serous fluid. There is also intlItration with eosinophils and
round cells.
Site of origin. Multiple nasal polypi always arise from the lateral wall of nose,
usually from the middle meatus. Common sites are uncinate process, bulla ethmoidalis,
ostia of sinuses, medial surface and edge of middle turbinate. Allergic nasal polypi almost
never arise from the septum or the floor of nose.
Symptoms
1. Multiple polypi can occur at any age but are mostly seen in adults.
2. Nasal stuffiness leading ro total nasal obstruction may be the presenting symptom.
3. Partial or total loss of sense of smell.
4. Headache due to associated sinusitis.
5. Sneezing and watery nasal discharge due to associated allergy.
6. Mass protruding from the nostril.
Signs.
On anterior rhinoscopy, polypi appear as smooth, glistening, grape-like masses
often pale in colour. They may be sessile or pedunculated, insensitive to probing and do
not bleed on touch. Often they are multiple and bilateral. Long-standing cases present with
broadening of nose and increased intercanthal distance. A polyp may protrude from the
nostril and appear pink and vascular simulating neoplasm. Nasal cavity may show purulent
discharge due to associated sinusitis.

16. Probing of a solitary ethmoidal polyp may be necessary to differentiate it from
hypertrophy of the turbinate or cystic middle turbinate.
Diagnosis.
Diagnosis can be easily made on clinical examination. CT scan of paranasal sinuses is
essential to exclude the bony erosion and expansion suggestive of neoplasia. Simple nasal
polypi may sometimes be associated with malignancy underneath, especially in people
above 40 years and this must be excluded by histol gi cal examination of the suspected
tissue. CT scan also helps to plan surgery.
Treatment
Conservative
1. Early polypoidal changes with oedematous mucosa may revert to normal with
antihistaminics and control of allergy.
2. A short course of steroids may prove useful in case of people who cannot tolerate
antihistaminics and or in those with asthma and polypoidal nasal mucosa. They
may also be used to prevent recurrence after surgery. Contra ind ications to use of
steroids, e.g. hypertension, peptic ulcer, diabetes, pregnancy and tuberculosis
should be excluded.
Surgical
1. Polypectom)t. One or two polyps which are pedunculated can be removed . with
snare. Multiple and sessile polypi require special forceps.
2. Intranasal ethmoidectomy. When polypi are multiple and sessile they require
uncapping of the ethmoidal air ce lls by intranasal route, a procedure called
intranasal ethmoidectomy.
3. Extranasal ethmoidectomy. This is indicated when polypi recur after intranasal
procedures and surgical landmarks are ill-defined due to previous surgery.
Approach is through the medial wall of the orbit by an external incision, medial to
medial canthus.
4. Transantral ethmoU:l.ectomy. This is indicated when infection and polypoidal
changes are also seen in the maxillary antrum. In this case, antrum is opened by
Caldwell-Luc approach and the ethmoid air cell approached through the medial
wall of the antrum. This procedure is also superceded by endoscopic sinus surgery.
5. Endoscopic sinus surgery. These days, ethmoidal polypi are removed by
endoscopic sinus surgery more popularly called FESS (functional endoscopic sinus
surgery). It is done with various endoscopes 0o ,30o and 70° angulation. Polypi can
be removed more accurately when ethmoid cells are removed, and drainage and
ventilation provided to the other involved sinuses such as maxillary, sphenoidal or
frontal.

17. Antrochoanal Polyp
This polyp arises from the mucosa of max illary antrum near its accessory ostium,
comes out of it and grows in the choana and nasal cavity. Thus it has three parts.
a) Antral: which is a thin stalk.
b) Choanal: which is round and globular.
c) Nasal: which is flat from side to side.
Etiology.
Exact cause is unknown. Nasal allergy coupled with sinus infection is incriminated.
Antrochoanal polypi are seen in children and young adults. Usually they are single and
unilateral.
Symptoms.
Unilateral nasal obstruction is the presenting symptom. Obstruction may become bilateral
when polyp grows into the nasopharynx and starts obstructing the opposite choana. Voice
may become thick and dull due to hyponasality. Nasal discharge, mostly mucoid, may be
seen on one or both sid es.
Signs.
As the antrochoanal polyp grows posteriorly, it may be missed on anterior
rhinoscopy. When large, a smooth greyish mass covered with nasal discharge may be seen.
It is soft and can be moved up and down with a probe. A large polyp may protrude from
the nostril and show a pink congested look on its exposed part.
Posterior rhinoscopy may reveal a globular mass filling Large benign and
malignant tumours the choana or the nasopharynx. A large polyp may hang down behind
the soft palate and present in the oropharynx
Differential diagnosis
1. A blob of mucus often looks like a polypi but it would disappear on blowing the
nose.
2. Hypertrophied middle turbinate is differentiated by its pink appearance and hard
feel of bone on probe testing.
3. Angiofibroma has history of profuse recurrent epistaxis. It is firm in consistency
and easily bleeds on probing.
4. Other neoplasms may be differentiated by theIr fleshy pink appearance, friable
nature and their tendency to bleed.

18. X-rays of paranasal sinuses may show opacity of the involved antrum. X-ray,
(lateral view) soft tissue nasopharynx, reveals a globular swelling in the postnasal space.
It is differentiated from angiofibroma by the presence of a column of air behind the polyp.
Treatment.
An antrochoanal polyp is easily removed by avulsion either through the nasal or oral route.
Recurrence is uncommon after complete removal. In cases which do recur, Caldwell-Luc
operation may be required to remove the polyp completely from the site of its origin and
to deal with co-existent maxillary sinusitis. These days, endoscopic sinus surgery has
superceded other modes of polyp removal. Caldwell-Luc operation is avoided .
Some Important Points to Remember in a Case of Nasal Polypi
1. If a polypus is red and fleshy, friable and has granular surface, especially in older
patients, think of malignancy.
2. Simple nasal polyp may masquerade a malignancy underneath. Hence all polypi
should be subjected to histology.
3. A simple polyp in a child may be a glioma, an encephalocele or a
meningoencephalocele. It should always be aspirated and fluid examined for CSF.
Careless removal of such polyp would result in CSF rhinorrhoea and meningitis.
4. Multiple nasal polypi in children may be associated with mucoviscidosis.
5. Epistaxis and orbital symptoms associated with a polyp should always arouse the
suspicion of malignancy.
b. Sinusitis15
Definition
Sinusitis defines as mucul inflammation of paranasal sinus. Sinusitis mostly
caused by rhinitis, so that can be called rhinosinusitis. Rhinosinusitis mostly caused by
common cold which is a virus infection and bacterial infection can be included then. If
sinusitis occur in several sinus it’s called multisinusitis, while occur in all sinus it’s called
parasinusitis. Mostly sinus that occur is ethmoidal sinus and maxillary sinus.
Etiology
Some etiology and predispotition factors are Upper Respiratory Tract Infection
cause by virus, rhinitis, nasal polip, abnormality anatomy structur such as septum deviation
or concha hypertrophy, obstruction of osteo-meatal complex, tonsil infection,
immunologic abnormalitiy, ciliary dyskinesia, and cystic fibrotic.
The other factor that relevant are environment pollution, cold air and dry, smoking.
This can make structural changes of cilia and damaged the cilia.

19. Pathophisiology
Normal sinus depend on osteomeatal complex (OMC) and mucociliary clearance
in OMC. Mucuos contain some antimicrobal substance and other substance that have a
function as body defence.
Location of organs that form OCM is near and if edema is happen, mucous that
face each other will be combined and lead to obstruction of ostium. As a result, negative
pressure happened in cavum sinus that cause transudation, start with serous. This condition
regarded as non-bacterial rhinosinusitis and can be recover in few days without medical
treatment.
If this condition continued, the secret that accumulated inside sinus can lead to
microorganisms grow and bacterial multiplication. Then, secret become purulent, this
condition called as bacterial acute rhinosinusitis and need a medical treatment.
If treatment fail, inflammation continue, lead to hypoxia and growth of anaerobe
bacteria occur. Mucous getting swollen and it can be continuously and lead to mucous
change become chronic such as hypertrophy, polipoid, or polip and cyst forming. If this
condition happen, it need surgical treatment
Symptoms
Mostly syptoms of sinusitis are nasal congestion, face pain, purulent secret and
usually post nasal drip happen. Fever and weakness usually happen.
Pain pressure in sinus area is characteristic of acute sinusitis and also can be
referred pain. If pain happen in cheeks it’s maxillary sinusitis and can lead to pain in teeth
and ears, pain between or behind eyes is ethmoidal sinusitis, pain in forehead is frontalis
sinusitis. The other symptoms are headache, hyposmia, anosmia, halitosis, post nasal drip
that can lead to cough.
In chronic sinusitis, the symptoms is not specific, sometimes one or two symptoms
that happen : chronic headache, post nasal drip, post nasal drip, chronic cough, throat
disorder, ears disorder caused by chronic obstruction of tuba Eustachius, pulmonary
disorder such as bronchitis or bronchiectasis. In child, post nasal drip can cause
gastroenteritis.
Diagnosis
Physical examination with anterior and posterior rhinoscopy, naso-endoscopy is
the most important to make a proper diagnosed. Specific sign is a pus in meatus medius
(maxillary sinusitis, anterior and frontal ethmoidal) or in superior meatus (posterior
ethmoidal sinusitis and sphenoidale). In acute rhinosinusitis can found mucuos edem and
hyperemic.
Support examination using CT-Scan is the most important. CT-scan is gold
standard to diagnose sinusitis because can evaluate anatomy structural of nose and sinus,

20. evaluate the disorder inside nose and sinus overall. Microbiological test can be do with
take a secret from superior/medial meatus to give a specific antibiotic.
Treatment
Antibiotic and decongestant are the first line therapy in acute bacterial sinusitis to
remove the infection and mucous swolling also can remove the ostium sinus obstruction.
In case of antibiotic resistance, we can give amoxicillin-kluvanat or cephalosporin 2nd
generation. In acute sinusitis, antibiotic given for 10-14 days despite the symptoms
disappear. In chronic sinusitis antibiotic given based on gram negative bacteria and aerob
bacteria.
Besides topical and oral decongestant, other treatment necessary are analgetic,
mucolytic, topical/oral steroids. Antihistamin not given routinely because anticholinergic
effect can make secret become thick.
c. Rhinitis17
Description
Rhinitis is defined as inflammation of the nasal membranes and is characterized by
a symptom complex that consists of any combination of the following: sneezing, nasal
congestion, nasal itching, and rhinorrheaThe eyes, ears, sinuses, and throat can also be
involved. Allergic rhinitis is the most common cause of rhinitis. It is an extremely common
condition, affecting approximately 20% of the population.
Although allergic rhinitis is not a life-threatening condition, complications can
occur and the condition can significantly impair quality of life, which leads to a number of
indirect costs. The total direct and indirect cost of allergic rhinitis was recently estimated
to be $5.3 billion per year. A 2011 analysis determined that patients with allergic rhinitis
averaged 3 additional office visits, 9 more prescriptions filled, and $1500 in incremental
healthcare costs in 1 year than similar patients without allergic rhinitis.
Etiology
- Onset usually in first 4 decades with declining tendency with advancing age
- Mean age onset approximately 10 years
- Predominant sex: Male = Female
Risk Factors
- Family history
- Repeated exposure to offending antigen
- Exposure to multiple offending allergens
- Presence of other allergies, e.g., atopic dermatitis, asthma, urticaria

21. - Non-compliance to appropriate therapeutic measures
Signs & symptoms
- Nasal stuffiness and congestion
- Rhinorrhea usually clear
- Pruritus of nose, eyes and palate
- Sneezing, often paroxysmal
- Injection and watering of eyes
- Postnasal drainage
- Mouth breathing
- Fatigue or malaise
- Dark circles under eyes, “allergic shiners”
- Transverse nasal crease from rubbing nose upwards
Causes
- Inhalant allergens:
1) Perennial: house dust mites, molds, animal dander, cockroach ◊ Seasonal:
tree, grass and weed pollens
2) Occupational: latex, plant products (such as baking flour), sensitizing
chemicals
Pathofisiology
Allergic rhinitis involves inflammation of the mucous membranes of the nose,
eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is involved,
and the other organs are affected in certain individuals. Inflammation of the mucous
membranes is characterized by a complex interaction of inflammatory mediators but
ultimately is triggered by an immunoglobulin E (IgE)–mediated response to an extrinsic
protein.
The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens
(proteins capable of causing an allergic reaction) has a genetic component. In susceptible
individuals, exposure to certain foreign proteins leads to allergic sensitization, which is
characterized by the production of specific IgE directed against these proteins. This
specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When
the specific protein (eg, a specific pollen grain) is inhaled into the nose, it can bind to the
IgE on the mast cells, leading to immediate and delayed release of a number of mediators.
The mediators that are immediately released include histamine, tryptase, chymase,
kinins, and heparin. The mast cells quickly synthesize other mediators, including
leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately

22. lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness,
tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to
increased secretions. Vascular permeability is increased, leading to plasma exudation.
Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated,
leading to sneezing and itching. All of these events can occur in minutes; hence, this
reaction is called the early, or immediate, phase of the reaction.
Over 4-8 hours, these mediators, through a complex interplay of events, lead to the
recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils,
lymphocytes, and macrophages. This results in continued inflammation, termed the late-
phase response. The symptoms of the late-phase response are similar to those of the early
phase, but less sneezing and itching and more congestion and mucus production tend to
occur. The late phase may persist for hours or days.
Systemic effects, including fatigue, sleepiness, and malaise, can occur from the
inflammatory response. These symptoms often contribute to impaired quality of life.
Pathological Finding
- Nasal washing/scraping
- Eosinophils predominate
- Basophils
- May see mast cells
- Nasal mucosa
- Submucosal edema but intact without evidence of destruction
- Eosinophilic infiltration
- Granulocytes to lesser extent
- Increased amount of tissue water with poor staining of ground substance
- Congested mucous glands and gobl
Special Test
- Skin tests using suspected antigens. Either technique manifests a positive reaction
by inducing an expanding wheal and flare reaction. Special training recommended
and available treatment for anaphylaxis mandatory.
- Prick or puncture: a superficial injury to the epidermis with application of diluted
test antigen
- Intradermal: Introduction of diluted material between layers of skin raising a 4 mm
wheal using a 25 or 27 gauge needle Radioallergosorbent test (RAST)
- More expensive and used especially in cases where skin testing not practical, e.g.,
in atopic dermatitis and dermatographia Audiometry

23. - For deficits and baseline evaluation
- Rhinoscopy: particularly useful to visualize intra-nasal anatomy, posterior
pharyngeal structures including adenoids and larynx
Imaging
Sinus radiographs when indicated. Check for complete opacity, fluid level and
mucosal thickening. Sinus imaging using CT may be preferable.
Laboratory
- CBC with differential. May have slight increase in eo- sinophils but often normal
with uncomplicated rhinitis.
- Nasal probe smear with cytologic exam for eosinophils • Increase IgE level.
Determine specific allergen sensitiv- itchy with allergen skin testing or RAST
11. Therapy and first treatment for patients with olfactory disorders?
Treatment of Olfactory1
Treatment of olfactory dysfunction
Any treatment of olfactory disorders must first treat the specific causative abnormality
if it has been identified from diagnostic tests, history, and physical examination.
Local nasal and/or sinus conditions should be optimally managed with saline lavage,
decongestants, antihistamines, antibiotics, and/or nasal and systemic steroids, if
applicable. Polyps and sinus disease that are resistant to medical management should be
surgically addressed to remove the conductive defect. Care must be exercised during
surgery to avoid damage to the olfactory regions.
Aggressive treatment of these disorders, if present, provides a good chance of
improvement. In general, conductive olfactory losses are the most amenable to treatment.
A few of the sensorineural olfactory defects also have specific treatments, but these
are fewer and have less chance of success. Generally, viral processes that damage the
olfactory neuroepithelium, sarcoidosis, and multiple sclerosis do not have specific
remedies; however, steroids may be administered in an attempt to limit the inflammation.
Endocrine disturbances may be addressed by administration of the deficient hormone,
as with hypothyroidism. Control of diabetes mellitus may slow neural degeneration of the
olfactory system. However, in a study of 12 males with Kallmann syndrome, Gong and
Gao stated that, while the condition can be effectively treated with the administration of
human chorionic gonadotropin (hCG), human menopausal gonadotropin (hMG), and
testosterone undecanoate, there is currently no effective therapy for the olfactory
dysfunction occurring in this disease.

24. Idiopathic cases of olfactory loss are not amenable to specific treatment, although some
unproven remedies have been attempted. The best known of these is zinc sulfate. It has not
been proven beneficial and is generally regarded as ineffective.
Other unproven remedies include pharmacologic doses of vitamins, topical steroids,
and tricyclic antidepressants (for their effect on CSF catecholamines).
A viral URTI can cause extensive scarring and replacement of the olfactory
neuroepithelium with respiratory epithelium, but studies suggest that stem cells remain,
allowing for potential regeneration of the olfactory epithelium. Recovery of smell in these
cases can take weeks to months and, in some instances, may never occur. It is now known
that olfactory training is safe and effective therapy for postinfectious olfactory loss. This
method involves the patient choosing 4 known odors and intentionally sniffing these same
4 odors twice daily. A recent randomized, controlled study showed improved olfactory
function after 18 weeks, particularly in patients who started olfactory training within the
first 12 months after onset. Eliminating toxins (eg, cigarette smoke, airborne pollutants)
may help.
A literature review by Pekala et al indicated that olfactory training may be an effective
treatment in patients with olfactory loss resulting from multiple etiologies, with
improvements reported in discrimination between and identification of smells, although
not in thresholds of odor detection.
Overall, the patient with olfactory disorders needs reassurance that these generally are
not life-threatening problems and that many other individuals experience them. In some
patients, psychiatric evaluation and treatment may be warranted. Most importantly, the
physician is responsible for warning the patient with olfactory disorders of the hazards
associated with the inability to smell odors such as smoke, natural gas leaks, and spoiled
food. Smoke detectors, as well as natural gas and propane gas detectors, are commercially
available to help eliminate such risks.

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