[UNIT 7]: M.

03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY

Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

OUTLINE B. NORMAL CT SCAN

I. NORMAL SINUS ANATOMY AND FUNCTION
II. OLFACTORY DISORDERS
III. RHINITIS
*NOTE: Section I of this trans is lifted from 2022 Trans*

I. NORMAL SINUS ANATOMY AND FUNCTION

A. SINUSES
Ø True function up to this day is still unknown
Ø Presumed Functions:
• Humidifies and filters the air we breathe
• Acts as shock absorber to the head in setting of trauma
օ Example: If you look at the forehead area, there is a
frontal sinus there. Imagine if there is no sinus, force
in the forehead would directly be delivered in the
brain.
օ The sinus intervenes and acts as a shock absorber of
all the pressure so brain and other underlying Figure 2. Coronal CT Scan showing the Maxillary Sinus (arrows).
structure are not hurt. Circle: Shows the narrow outflow of the sinus - this can allow even the
smallest amount of edema or congestion to result in obstruction that
can develop into an acute sinus process.

Figure 1. Sinuses. Coronal View (Left) and Sagittal View (Right)

Ø Location of a patient’s pain can dictate and guide in determining

the location of the underlying disease
Ø 4 paired sinuses:
• Frontal (forehead) Sinus
օ Situated behind the forehead Figure 3. Coronal CT Scan showing the Sphenoidal Sinus
Star: Location of the optic nerve: dehiscent 6% of the time on CT scans
օ Starts to be produced right around teenage years, and
– acute sphenoid sinusitis can spread to the optic nerve causing
then finishes shortly after puberty
blindness, if there is no bone in that location
օ Manifests as frontal tenderness if infected; if it is Arrow: Location of the carotid artery – 22% of the time, the bone
severe – swelling and redness overlying the skin of overlying the carotid artery can be missing
that area that may suggest an underlying process C. SINUS EPITHELIUM
called Pott’s Puffy Tumor (a chronic osteomyelitis of
the frontal bone)
• Ethmoid Sinus
օ Honeycomb of air cells situated right next to the eyes
օ Infection in the sinus can easily spread into the eyes
causing infections, such as orbital cellulitis or orbital
abscess (a collection of pus around the orbit, which
is a surgical condition; hence, need to be drained)
• Maxillary Sinus
օ Largest and first sinus that is present at birth
օ If there is unilateral maxillary sinusitis, it is important
to rule out an odontogenic process due top its
intimate relationship to the underlying upper teeth Figure 4. Sinus Epithelium through the Maxillary Sinus
• Sphenoid Sinus
օ Manifests as occipital headaches or retroorbital Ø Mucociliary clearance
headaches • A key host defense mechanism
օ very rarely, may also present with frontal headaches • Clears locally produced debris, excessive secretions,
օ serves as a gateway to the a sella turcica, where the inhaled particles, infectious agents
pituitary gland is located • Cilia + Mucus layer
Ø Ciliary Beat
• Normal Cilia: coordinated beating (metachrony)

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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY
Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

Figure 8. Accessory opening in the Maxillary Sinus

Figure 5. Normal Ciliary Beat

Moves pathogens in an anterior-to-posterior direction (metachrony)

Ø Abnormal Cilia: ineffective, decreased beating (dyskinesia)

• E.g. Kartagener’s syndrome

Figure 9. Mucus Recirculation

Mucus leaves the normal sinus opening (star) then recirculates back
into the accessory opening square, which is a setup for recurrent
maxillary sinusitis, chronic maxillary sinusitis, or that feeling of a thick
postnasal drip (thick mucus being dislodged posteriorly)

E. FLOW PATTERN: FRONTAL SINUS

Figure 6. Dyskinesia: can result to stagnation of allergens, bacterial

pathogens, particles, debris, which is a setup for chronic sinusitis
(ciliary defense is no longer functioning because the mucociliary
mechanism is ineffective)

D. FLOW PATTERN: MAXILLARY SINUS

Figure 10. Frontal Sinus Mucocilary Clearance (green) and Mucus

Recirculation (purple)
Ø Green arrows represent the mucociliary clearance; wherein,
mucus goes up the medial wall, flows along the roof, and mucus
exits down the lateral wall of the sinus
Ø Purple arrows represent mucus recirculation, which occurs in
10% of cases
Ø The frontal sinus normally has mucus recirculation

Figure 7. Flow Pattern for Mucociliary Clearance

Mucociliary clearance does not only occur in the nose, it also takes
place in each sinus. In the figure showing the left maxillary sinus, even
though there is an opening up to the top, the sinus extends all the way
down to the nasal floor and sometimes even lower in adults, so the
sinus still has to move mucus from that floor up to that natural opening Figure 11. Obstruction (red arrow) causing increased recirculation
(purple)

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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY
Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

• Sweet like caramel

• Minty like peppermint
• Toasted and latte like popcorn
• Pungent like cigar smoke
• Thick odor like rotten meat
Ø Consider the strength of the smell:
• Mild
• Moderate
• Strong

A. TERMINOLOGIES
• Inability to detect qualitative
olfactory sensations; absence of
smell function
Anosmia
• A person with anosmia will not be
able to perceive an odor even in a
presence of a stimulus.
Partial anosmia Ability to perceive some (but not all) odors
Figure 12. If there is an obstruction to both outflows, a modified Lothrop
procedure can be performed, which is the removal of the central Decreased sensitivity to odors, such that
segment (rectangle) (A) to repair Mucocilary Clearance (B) Hyposmia or Microsmia you have to present a stronger stimulus for
the person to detect the odor
F. SINUS DRAINAGE PATHWAYS • Reflects increased sensitivity to
common odors; heightened response
to an odor.
• It is not an increased ability to smell.
• Reported in some conditions
Hyperosmia associated with a change in hormone
balance, such as in pregnancy and
Addison’s disease, as well as
migraine, drug withdrawal, epilepsy,
multiple chemical sensitivity, and
psychosis
Distorted or perverted smell perception to
Dysosmia/ Cacosmia/
odor stimulation, such that a person will
Parosmia
perceive a stimulus in a different way
Dysosmic sensation perceived in the
Phantosmia/ Olfactory absence of an odor stimulus, such that a
hallucination person will perceive the odor in the
Figure 13. Sinus Drainage Pathways absence of a stimulus
Ø The anterior and posterior systems drain from different • Inability to recognize an odor
locations sensation, even though olfactory
• Anterior Pathway: drains the frontal, anterior ethmoid, and processing, language, and general
maxillary sinus intellectual functions are essentially
Olfactory agnosia
• Posterior Pathway: drains posterior ethmoid and sphenoid intact as in some stroke patients,
sinuses • so the patient can perceive the smell
Ø In performing a nasal endoscopy, seeing where the drainage is but cannot identify or recognize that
with respect to the Eustachian tube, in some ways can help smell
figure out where the disease is without doing a CT scan Presbyosmia Decline in a sense of smell with age
• If you see mucus draining ABOVE the Eustachian tube Osmophobia A dislike or fear of certain smells
orifice, then that process has to be originating from the
posterior ethmoid or the sphenoid process B. INCIDENCE
• If the mucus is seen draining BELOW the Eustachian tube Ø Occurs more common in men who lose their ability of smell in
orifice, the disease process has to be originating from the earlier life
frontal, anterior ethmoid, or maxillary sinus Ø Chemosensory loss is age dependent leading to presbyosmia

Please read on M.04S Acute Sinusitis C. ETIOLOGY

and M.05S Chronic Rhinosinusitis. Ø All pathological process at any level along the olfactory
pathway (nasal cavity to the brain)
II. OLFACTORY DISORDERS 1. CONDUCTIVE
Ø In assessing olfaction, we have to consider the quality of the • Transport loss
smell and the type and the strength of the odor. • Refer to conditions that interfere with access of odorants
Ø Basic smells: to the olfactory neuroepithelium, like viral infection,
• Fragrant or floral bacteria or allergic rhinitis, nasal polyps, septal deviation
• Fruity • Any abnormalities that cause obstruction of the nasal
• Citrus passages
• Woody or Resinous like pine
• Chemical like bleach 2. SENSORY

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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES
Dr. Adaci
03.07.2022
• Damage to the olfactory neuroepithelium, central tracts,
and its connections, which are usually triggered by viruses,
airborne toxins, tumors, seizures, drugs, and radiation
therapy
3. NEURAL LOSS
• Damage of the central olfactory pathway, usually attributed
to trauma, neurodegenerative diseases, alcoholism,
smoking, AIDS, and neoplasms
• Difficult to classify an olfactory disorder into one of these
classes because both blockage of airflow to the receptors
and damage to the receptors or other elements of the
olfactory neuroepithelium can be present.
• Viruses may damage olfactory nerve.
o Parainfluenza virus type 3 is especially detrimental to
olfaction
• HIV is associated with subjective distortion of smell/taste.
D. TYPES
1. CONDUCTIVE OLFACTORY DISORDERS
Ø Conditions which can decrease the nasal airflow and block the
access of odorants to the olfactory epithelium
Ø Patients may still have some retronasal airflow, allowing the
ability to detect the flavor of food
Ø Causes of decreased nasal airflow include nasal septal
deformities, nasal polyposis, tracheostomy (the airflow doesn’t
pass through your nose), other nasal cavity tumors, post-op
adhesions following nasal surger
2. SENSORINEURAL OLFACTORY DISORDERS
Ø Due to damage anywhere from the olfactory epithelium in the
nose up to the central olfactory pathway
Ø This may be due to different factors:
a. UPPER RESPIRATORY INFECTIONS
• Loss of olfaction after a URI is one of the most
common causes of smell disorders
• Olfactory dysfunction during a URI can initially be
conductive during the active stage of the infection,
but persistence of loss of smell after resolution of
other symptoms indicates sensorineural injury to
the olfactory epithelium, especially with a long-
standing inflammatory disease.
b. HEAD TRAUMA
• Often results in smell loss, particularly where rapid
acceleration/deceleration injury to the brain occurs
(i.e., coup/contrecoup injury)
• Prevalence is 15%
o Proportional to the severity of the injury
• Common mechanisms include:
o Disruption from shearing forces of the
olfactory fila through the sinonasal tract
o Direct contusion and ischemia to the olfactory
bulb and frontal and temporal poles
• Blunt trauma to the occiput, which is nearer your
olfactory cortex
o Produce greater olfactory vs. trauma to the
front of the head
• Loss of smell is usually, but not always, immediate,
and it may take a while for the patient to recognize
the presence of the dysfunction of the smell.
c. TUMORS AND MASS LESIONS
• along the olfactory pathway.
• A number of tumors in and around the olfactory
bulbs or tracts (olfactory groove meningiomas,
frontal lobe gliomas, suprasellar ridge meningiomas
(arises from the dura of the cribriform plate), mesial
temporal lobe tumors) can cause olfactory
disturbance.
• Most lesions around the olfactory region can result
in Foster- Kennedy Syndrome.
Gapuz, Sunio, Velasquez, D.
OTORHINOLARYNGOLOGY
Saint Louis University
School of Medicine
o Ipsilateral anosmia
o Ipsilateral optic atropy
o Contralateral papilledema
d. CONGENITAL LOSS
• 3% of anosmia, usually an isolated finding
• Patients often present during their preteen or
teenage years with an inability to smell and is often
discovered by family members.
• Patients with congenital lack of olfactory ability may
not recognize their olfactory dysfunction and have
no recollection of detecting odors.
• May have distinct food preferences due to their
inability to appreciate the flavor of food while
retaining the ability to detect the fundamental taste
sensations from the taste buds
e. TOXINS
• Olfactory dysfunction attributed to toxin exposure is
relatively low (2%).
• Environmental pollutants, specific metal fumes like
cadmium (most common), chromium, nickel,
mercury and lead, gas exposure from industrial
plants, solvents including toluene and paint solvents,
tobacco smoke.
• Mechanism of injury:
o Olfactory receptor neurons are in direct
contact with the environment, leaving them
vulnerable to inhaled toxins.
o By-products of metabolism of the odorants by
‘Cytochrome P450 monooxygenase system’ in
the supporting cells damage olfactory
epithelium.
o Cytochrome P450 monooxygenase detoxify
inhaled or systemic substances presumably to
protect the olfactory neurons and the central
nervous system to process odorant molecules
for receptor activation; however, by-products
of these enzymes may include toxic
metabolites which themselves may damage
the olfactory epithelium.
• Damage to the olfactory epithelium
o Acute – high levels of toxin exposure
o Chronic – low level exposure, causing more
gradual olfactory decline
• For tobacco smoke, exposure is associated with
hyposmia in active smokers due to increased
olfactory receptor neuron apoptosis.
f. AGE
• <65 years – 1-2% of population has major difficulty
in smelling
• 65-80 years – 60% of the population experiencing a
demonstrable decrement in the ability to smell, 25%
anosmic
• >80 years – 80% with olfactory impairment, 50%
anosmic
• There is a combination of damage over the years,
and a single event, such as a bad cold, can be a
precipitating event.
• Age-related changes in smell function are due to:
o Damage to the olfactory receptors
o Decreased activity of basal cell to regenerate
o Replacement of olfactory epithelium by
respiratory epithelium
o Occlusion of the foramina of the cribriform
plate
§ Pinching off the axons of the olfactory
receptor cells as they enter the brain
cavity
o Decreases in number of glomeruli within the
olfactory bulb
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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY
Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

g. NEURODEGENERATIVE DISORDERS Ø Possible bacterial infections: characterized by mucopurulent

• Patients with Alzheimer and Parkinson disease: 90% secretions
exhibit olfactory dysfunction in the early stages of Ø Noninfectious rhinitis has been classified as either allergic or
the disease non-allergic
• Olfactory loss may be the first clinical sign. Ø Occurs most commonly as allergic rhinitis
h. EPILEPSY AND MIGRAINE A. ALLERGIC RHINITIS (AR)
• Olfactory auras, also described as hallucinations, Ø 20% of nasal inflammation
are usually rare and consist of sudden unexplained Ø Chronic or recurrent IgE-mediated inflammation of nasal
sensations of smell that are usually, but not always, mucosa which is an immune reaction to specific external
unpleasant, and are isolated events. factors known as allergens
Ø Type 1 hypersensitivity response to an antigen (allergen) in a
E. EVALUATION genetically susceptible person resulting to a local vasodilation
Ø History: focus on targeting an underlying cause and increased capillary permeability
Ø Complete physical examination Ø Presenting symptoms such include:
Ø Thorough head and neck, neurological examination • Nasal obstruction
Ø Cognition and mood to rule out other psychological problems • Clear nasal discharge (anterior and posterior)
Ø Signs of systemic diseases • Nasal congestion
Ø Nasal endoscopy to properly assess the nose and paranasal • Post-nasal drainage
sinuses • Sneezing
Ø Laboratory work-up • Nasa itching
Ø Smell identification test • Reduced sense of smell
Ø Imaging of the nose and paranasal sinuses • Eye involvement (ocular pruritus, watery eyes)
Ø Immune reaction to specific external factors known as
F. TREATMENT allergens
1. CONDUCTIVE ANOSMIA CLASSIFICATIONS OF AR
Ø Main goal of management is to improve nasal airflow to Ø Seasonal vs. Perennial
improve the transport of odorants up to the neuroepithelium. • Seasonal – symptoms appear in or around a particular
Ø Treat underlying cause, like doing surgery to remove season (e.g pollen grains)
obstruction in cases of medical to nasal polyps, and surgery for • Perennial – symptoms are present throughout the year
septal mediations to improve the airflow. (e.g dust mites, insect parts, cockroaches, animal
Ø Humidify the nasal cavity to improve airflow and ciliary danders)
transport. Seasonal Perennial
Ø Topical or systemic steroids to manage anosmia are also
Intermittent (cyclical Persistent (year-round
helpful.
exacerbation) symptoms)
• Conductive and sensorineural olfactory losses are often
Outdoor allergens Indoor allergens
distinguishable using a brief course of systemic steroid
• Tree pollinates (Spring) • House dust mites
therapy since patients with conductive impairment usually
• Grasses (Early summer) • Animal dander
respond positively to a short-term steroid treatment.
Ø Proper allergy management to improve symptoms of allergic • Weeds (Late summer) • Molds, cockroaches
rhinitis Table 1. ARIA Classification of Allergic Rhinitis (Old)
Ø Control of bacterial infection if needed are also some measures
to improve airflow and the transport of odorants. Ø Intermittent vs. Persistent
2. SENSORINEURAL IMPAIRMENT • Depending on the duration of symptoms
Ø More difficult to manage • Intermittent – symptoms of less than 4 days a week OR
Ø Prognosis for patients suffering from long standing total loss less than 4 consecutive weeks
due to upper respiratory illness or head trauma is poor • Persistent – symptoms last for more than 4 days a week
Ø Patients who give up smoking typically have dose-related AND for more than 4 weeks
improvement in olfactory function and flavor sensation over
time. Ø Mild vs. Moderate to Severe
• Depends on the regeneration of neuroepithelium • Depending on the severity of the symptoms
Ø CNS tumors that impinge on olfactory bulbs and tracts can Mild Moderate to Severe
often be resected with significant improvement in olfactory ALL of the following: ONE OR MORE of the following:
function ü Normal sleep ü Sleep disturbance
Ø Epilepsy and migraine is suspected, course of antiepileptic or ü No impairment of daily ü Impairment of daily
antimigraine medications may prove beneficial activities, sports and leisure activities, sports and leisure
Ø Systemic/Topical corticosteroids ü No impairment of work and ü Impairment of work and
Ø Humidification school school
• Measures to improve the airflow and supportive measures ü Symptoms present but not ü Troublesome symptoms
that are necessary to protect the persons with troublesome
sensorineural impairment from harm Table 2. Mild vs Moderate to Severe AR

III. RHINITIS
Ø Inflammation and swelling of the mucous membrane of the
nose
• Characterized by runny nose/abundant nasal secretions
and nasal obstruction/ stuffiness/ congestion
• Usually caused by common cold or seasonal allergy
• Viral etiology: Rhinovirus and parainfluenza virus

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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY
Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

DIAGNOSTICS
Ø Detailed history and complete PE
Ø Anterior rhinoscopy with the following findings:
• Pale gray, dull red or red turbinates
• Boggy turbinates
• Minimal to profuse watery to mucoid nasal discharge
Ø Nasal endoscopy whether rigid or flexible
• For the complete assessment of nasal cavity from the
opening to the nasopharynx
Ø Percutaneous skin test
Ø Allergen-specific IgE Antibody Test (e.g Radioallergosorbent
Test or RAST)

TREATMENT
Figure 14. ARIA Guidelines: Classification of Allergic Rhinitis
(Summary)
PRECIPITATING FACTORS
Ø Allergens present in the environment
• House dust and dust mites, feathers, tobacco smoke,
insects, animal dander, pollens
Ø Abnormalities in nasal physiology
Ø Disturbances in normal nasal cycle
PREDISPOSING FACTORS
Ø Genetic predisposition: 50% of AR patients have a positive
family history of AR
Ø Endocrine
Ø Puberty
Ø Pregnant states and post-partum stages/ menopausal
Ø Age/Sex
Ø Psychological
Ø Degree of pollution/ Humidity and temperature differences/
Temperature changes
Ø IgA Deficiency
PATHOGENESIS
Ø In a genetically predisposed individual:
• Inhaled allergen à IgE production à IgE binds to
basophils and mast cells by the Fc end à Exposure
allergens bind to Fab fragment à Mast cell degranulation
à Chemical mediators which then cause vasodilation,
mucosal edema, infiltration of eosinophils, excessive
secretion, smooth muscle contraction
SIGNS
Ø Nasal signs:
• Allergic salute – transverse nasal crease, black line in the
dorsum of the nose
• Pale and edematous nasal mucosa, swollen turbinates
• Thin, watery or mucoid discharge
Ø Ocular signs:
• Edema of lids, congestion, cobble stone appearance of
conjunctiva
• Allergic Shiners – dark circles under eyes
Ø Otologic signs:
• Eustachian tube blockages, retracted tympanic membrane,
serous otitis media
Ø Pharyngeal signs:
• Hyperplasia of submucosal lymphoid tissue, granular
pharyngitis
• Mouth breathing leading to orthodontic changes
Ø Laryngeal signs:
• Hoarseness of voice due to edema of vocal cords
Ø Environmental Control Measures:
• Avoidance or riddance of allergens
• Minimize exposure to the outdoors with expected high
pollen count
• Indoor allergen avoidance/ eradication (e.g dust mites)
• Reduction of indoor fungal exposure
• Removal is the most effective way to manage animal/
cockroach sensitivity
Ø Pharmacotherapy: Treatment with drugs
a. Antihistamines
o Decrease rhinorrhea, sneezing, nasal itch
b. Sympathomimetics
o E.g. Pseudoephendrine and phenylephrine,
oxymetazoline
o Usually used in combination with antihistamines
which will cause vasoconstriction thereby
decreasing nasal congestion and edema
c. Corticosteroids
o Inhibit recruitment of inflammatory cells to reduce
inflammation of mucosa
o Prevents mediator release
o Manages late allergic phase and can be used safely
daily
o Systemic CS – short course during disabling attack
o Intranasal CS – prolonged use, gold standard in AR
management
d. Sodium Chromoglycate
o Stabilizes mast cells to prevent degranulation
o Prevents release of chemical mediators
e. Leukotriene Receptor Antagonist
o Anti-IgE
o Reduces inflammation, edema and mucous
secretions
Ø Immunotherapy:
• Allergen is given in gradually increasing doses until the
maintenance dose is reached
• Recommend if AR is refractory to pharmacotherapy or in
cases of severe AR
• Reduces the specific serum IgE level
• Decreases the basophil sensitivity
• Increases IgG blocking antibody level, thus preventing
allergen from reaching mast cells and subsequent mast
cell degranulation
Ø Adjunctive Therapy:
• Nasal saline irrigation/ Nasal douche
• Helps in cleansing the nasal cavity of allergens, mucous
and debris, humidification of the nose, relieving nasal
symptoms of AR

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 [UNIT 7]: M.03 DISEASES OF THE NOSE & PARANASAL SINUSES OTORHINOLARYNGOLOGY
Dr. Adaci Saint Louis University
03.07.2022 School of Medicine

B. NON-ALLERGIC RHINITIS 6. Physiologic changes induced by pregnant state or menopause in

Ø Chronic rhinitis symptoms of nasal congestion, rhinorrhea, females.
post-nasal drainage in the absence of identifiable allergen, ACBACB
structure abnormality or sinus disease ANSWERS
Ø Distinguished from allergic rhinitis due to consistent presence
of symptoms, lack of nasal or ocular pruritus TRUE/FALSE
Ø Possible triggers: Strong fragrances, tobacco, perfume, 1. Persistent AR is characterized by symptoms of less than 4 days a
changes in temperature, cleaning products week OR less than 4 consecutive weeks.
Ø Divided into categories depending on the causative agent: 2. AR presents as a type II hypersensitivity reaction
1. INFECTIOUS RHINITIS 3. Adjunctive therapy for AR can be done using nasal douche.
Ø Viral etiology 4. Nasal rhinoscope is used to completely assess the nasal opening up
Ø Rhinovirus, Respiratory syncytial virus, Parainfluenza, Influenza, to the nasopharynx.
Adenovirus and Enterovirus 5. ACE inhibitors can be a trigger for non-allergic rhinitis.
2. VASOMOTOR RHINITS 6. A positive family history of AR is a predisposing factor for the
Ø Aka Non-allergic Rhinopathy disease.
Ø Chronic nasal symptoms that are not immunologic or infectious 7. Perennial AR is triggered by outside allergens such as pollens, grass
in origin and are not associated with nasal eosinophilia and weeds.
Ø Possible triggers: Changes in climate, strong odors, pollutants,
exercise FFTFTTF
3. HORMONE INDUCED RHINITIS ANSWERS
Ø Hormonal imbalance usually due to pregnancy, puberty,
menstruation, hypothyroidism IDENTIFICATION:
Ø Physiologic changes in pregnancy like vascular pooling and 1. Distorted or perverted smell perception to odor stimulation
plasma leakage usually exacerbate preexisting rhinitis in 1/5th 2. Damage of the central olfactory pathway
of pregnancy 3. Due to damage anywhere from the olfactory epithelium in the nose
4. OCCUPATIONAL RHINITIS up to the central olfactory pathway
Ø Rhinitis in the workplace due to inhaled irritants
Ø usually concurrent with occupational asthma 3. Sensorineural olfactory Disorder
5. DRUG-INDUCED RHINITIS 2. Neural loss
Ø AR during intake of medications 1. Dysosmia/ Cacosmia/ Parosmia
Ø Antihypertensives like ACE inhibitors and beta blockers ANSWERS
Ø NSAIDs
Ø Oral Contraceptives
6. RHINITIS MEDICAMENTOSA
Ø Rebound congestion of the nose due to prolonged use of nasal
sympathomimetics (e.g oxymetazoline) over 5 to 7 days
Ø This desensitizes the alpha receptors in the nose
Ø Treatment: Intranasal corticosteroids
7. NONALLERGIC RHINITIS OF EOSINOPHILIA SYNDROME
(NARES)
Ø Perennial disorder usually in middle aged adults
Ø Rhinitis with approximately 10-20% eosinophils on nasal smear
in the setting of negative assessment of aeroallergen-specific
IgE on allergen skin testing
Ø Responds well with intranasal CS or intranasal antihistamines

C. ATROPIC RHINITIS RHINITIS (AR)

Ø Rhinitis sicca or ozena
Ø Mucosal colonization with Klebsiella ozanae and other
organisms
Ø Nasal mucosa degenerates and loses mucociliary function
Ø Presents with foul smell as well as yellow/green nasal crusting
with atrophy and fibrosis of mucosa
Ø Anosmia
Ø Treatment: Intranasal CS

CHECKPOINT
MATCHING TYPE:
A. Allergic Rhinitis
B. Non-Allergic Rhinitis
C. Atrophic Rhinitis
1. It is caused by IgE-mediated hypersensitivity reaction.
2. Degeneration of nasal mucosa due to colonization of
microorganism.
3. Rebound congestion of nasal cavity due to overmedication of
oxymetazoline.
4. Intranasal CS is the gold standard of treatment.
5. Presence of yellow green nasal crusting with fibrosis of the nasal
mucosa.

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