ENT (supposedly) 2.

4 
Dr. Opulencia
Rhinitidis

Hello Classmates! As promised, the Rhinitidis! It’s from 2014A&B plus Probst NON-SPECIFIC CHRONIC RHINITIS
(especially yung mga hindi diniscuss ni Doc) and some reminders from the  Chronic inflammation of the nasal mucosa due to recurrent
30min lecture of Dr. Opulencia (hay). Again, sorry for my mistake! Happy acute inflammation and anatomic malformations such as septal
studying! –TQ  deviation, septal spur, polyps and tumors of the nasal cavity,
and adenoids of the nasopharnyx.
RHINITIS  Air pollutants and extreme weather changes could also bring
 Inflammation of the lining of the nose characterized by nasal about the condition.
congestion, sneezing and itching.  SYMPTOMS:
o Obstructed nasal breathing
Old classification: Allergic and Non-Allergic Rhinitis o Mucus nasal discharge
o Frequent throat clearing with occasional hoarseness
 Classifications:  TREATMENT:
a. Acute rhinitis (common cold) o Remove chronic irritants from the immediate environment
b. Non-specific chronic rhinitis o Surgical correction of anatomic abnormality
o Supportive measures such as decongestants (drops) or
ACUTE RHINITIS (COMMON COLD) nasal irrigation with saline solution
 Prevalent infectious disease WITHOUT postinfection immunity.
 RHINOVIRUS and CORONAVIRUS cause 50% of these cases. Allergic Rhinitis Non-Allergic Rhinitis
Minor causative agents are Influenza and adenovirus. Intermittent, mild Non-allergic rhinitis with
Boies: Nearly 200 viruses are responsible for the common cold Persistent, mild eosinophil syndrome (NARES)
 Transmission: airborne route (droplet infection). Moderate, severe Environmental
Persistent, moderate – severe Occupational
 Cold weather could also increase susceptibility to infection.
Hormonal
 Incubation period: 3-7 days. Drug-induced
 SYMPTOMS: Food-induced
o Initial dry stage symptoms: malaise (lethargy, headache, Emotional stress
fever), local discomfort in the nose &nasopharynx. Idiopathic
o Catarrhal stage symptoms:marked watery, initially serous
nasal discharge and nasal obstruction due to mucosal
swelling of turbinates. NON-ALLERGIC RHINITIS
 The viruses damage the cilia (mucociliary
transport system), thus hampering normal
clearing of secretions.  Resembles allergic rhinitis in clinical features, but there is no
o Viral damage to the epithelium increases risk for bacterial evidence that the patient has been previously sensitized
colonization which alters the consistency of the clear nasal  Pathogenesis is believed to involve neurovascular autonomic
discharge to being mucopurulent. disturbances in regulating the tonus of the nasal mucosal vessels
o Local and systemic symptoms subside in 1 week.
Boies: Vasomotor Rhinitis is a form of hypertrophic rhinitis with unknown
Boies: Start with nasal airway obstruction, excessive nasal discharge etiology although psychosomatic factors have been suggested. Two
sneezing and some coughing and general malaise with or without opposing forces are:
headache. Temperature maybe normal or slightly elevated. First stage Parasympathetic nerves that causes engorgement of the vascular bed
is limited to three to five days. The nasal secretions are at first watery with resultant congestion and increased mucous production
and profuse, then become mucoid, more viscid and scantier. The illness Sympathetic nerves that causes vasoconstriction which results to
may terminate at this point. In many patients however the illness nasal patency and decreased mucus production
progresses to a stage of secondary bacterial invasion characterized by
purulent rhinorrhea, fever and often a sore throat. A. Environmental Rhinitis
 Non-specific trigger in the environment
 TREATMENT: B. Cold-air Induced Rhinitis
o Supportive treatment: chamomile steam inhalation, light  Release of mast cell associated mediators (Non-IgE- it
baths, infrared therapy. means it’s not allergy) cause osmolality changes in
 Boies: Bed rest, isolation for two days, increased fluid the nasal secretion.
intake, administration of saline nose drops.
 Causes cholinergic responses.
o Decongestants (drops) should be used < 7 days due to risk
of tachyphylaxis& severe rebound swelling of nasal  Treatment: anticholinergic
mucosa. Boies: Sudden environmental temperature changes may stimulate nasal
congestion.
o Antibiotics are prescribed to patients with bacterial
C. Food Allergy or Gustatory Rhinorrhea
superinfection or paranasal sinus involvement.

Yours truly, TQ Page 1 of 6

  Hot and spicy food, alcohol, food colorants/
preservatives
D. Rhinitis Associated with Emotional States
 Anxiety, conflict, frustration, resentment, recollection
of humiliating and frustrating experiences
Boies: Fear and dejection results in shrinkage and pallor of the nasal mucosa
while anxiety, conflict, frustration, and resentment result in hyperemia,
swelling and hypersecretion.
E. Occupational Rhinitis
 Airborne agents present in the workplace such as
those in the laboratory (e.g. animals), grains, wood
dust, latex, and chemicals.
F. Hormonal Rhinitis
 During the 3rd trimester of pregnancy = status and
well-being of both the mother and baby should be
taken into account during management.
 Puberty
 Hypothyroidism
 Acromegaly
Boies: Estrogen stimulate vascular congestion of the nasal membranes.
During pregnancy, as the levels of estrogen rise, symptoms of nasal
congestion usually begin during the fourth to fifth month and progress to
term, paralleling the increased production of estrogen. Hypothyroidism could
also cause nasal obstruction and relief can be obtained with the use of
thyroid extract.
G. Drug-induced Rhinitis
 Topical ophthalmic agents (beta blockers in glaucoma)
 Aspirin for CVS problems
 Inhibit the COX pathway and shifts arachidonic acid
metabolism towards lipooxygenase production
resulting in increase of leukotrienes, which in turn
causes increased mucus secretion.
 NSAIDS
 Chlorpromazine (antipsychotic drug)
 Reserpine and ACEI (HTN)
 Viagra (BUT NOT PROVEN YET).
 Rhinitis medicamentosa (decongestants that treat
rhinitis can also cause rhinitis)
TREATMENT : The most important step is to eliminate the cause by
removing chronic irritants from the environment or by surgically
correcting any intranasal pathology. Supportive measures such as
decongestant nose drops or nasal irrigation with saline solution are
of only temporary benefit.
Boies: Rhinitis Medicamentosa – Results from the abuse of
sympathomimetic decongestant nose drops and nasal spray. After an initial
vasoconstriction, a secondary vasodilation (rebound vasodilation) occurs
which can make the nasal obstruction worse than before.
Other drugs that have been implicated: rauwolfia serpentinam alcohol,
tobacco and hashish.
SPECIAL PATIENTS WITH RHINITIS
A. RHINITIS IN CHILDREN
 Allergic rhinitis is part of ‘ALLERGIC MARCH’ and progressively
gets worse
 Starts at 2-3 y.o.,but is fully diagnosed at 6yoor at school-age.
 Infants do not have allergic rhinitis because this condition is
acquired. If infants do get rhinitis, this is because of early
exposure to food or milk formulas.
With <3, TQ
 Paradoxically, exposure to dogs, cats and endotoxin early in
childhood will decrease risk of allergic sensitization.
 Treatment:
o Children with severe and persistent symptoms are given
intranasal glucocorticoids (e.g. budesonide, mometasone,
fluticasone) because they offer greater topical activity
with lower systemic exposure and a better safety profile.
o Mometasoneis approved for >2 years old
o Fluticasone is approved for >4 years old
o Budesonide is approved for >6 years old
o Do NOT give intramuscular & oral steroids!!!
o Do NOT give topical vasoconstrictors because they have a
narrow margin of toxicity and therapeutic dose!!!
 Drixin (oxymetazoline) is a decongestant and
vasoconstrictor whichadults can use for a
maximum period of 1 week. Using it for >1 week
will cause rebound phenomenon.
 [Nelson] excessive use of Oxymetazoline in
children can cause profound neurologic
depression and using it for >3 days will cause
SEVERE rebound nasal congestion. Children who
are >6 years old can use oxymetazoline 0.05% 2-
3 drops or 1-2 metered sprays 2x/day.
o Do NOT give SEDATING FIRST GENERATION
ANTIHISTAMINES and LORATIDINE!!!
 Second generation antihistamines are the drugs
of choice because they cause less sedation.
ALWAYS REMEMBE! Allergic rhinitis is Ig-E mediated. A child is not
born with rhinitis. Usually nasal obstruction is the reason why they
are brought for consult.
Treatment: We avoid giving steroids to children.
B. RHINITIS IN THE ELDERLY
 Allergy is a less common cause of rhinitis for >65 years old.
 Atrophic rhinitis is more common. This is a condition of nasal
discomfort or ‘stuffiness’. The membranes appear dry, smooth,
shiny and with crusts. The cause is idiopathic. In severe cases,
there is secondary bacterial colonization which causes a foul
odor (ozena) that the patient cannot perceive due to
degeneration of the olfactory epithelium.
 Decongestants, particularly older antihistamines (1st gen) may
cause GI upset, nausea, constipation or diarrhea, and other
anticholinergic effects such as dry mouth, blurred vision and
urine retention.
 Treatment:
o Intranasal corticosteroid such as Beclomethasoneand
Flunisolide. These are administered as nasal sprays to
reduce systemic absorption and thus lower adverse effects.
o NON-sedating antihistamine (2nd gen) such as Loratidine
(Claritin) and Cetirizine are drugs of choice.
o Oxymetazolineshould be avoided. At high doses,
Oxymetazoline causes clonidine-like effects such as low BP
and low total peripheral resistance.
C. RHINITIS IN PREGNANCY
 Due to hormonal changes especially during the 2nd month AOG.
This is caused by estrogen-induced swelling of the mucosa with
nasal airway obstruction.
 Treatment:
o Medications may cross placenta during the 2nd and 3rd
trimesters so they are treated with topical antihistamines.
Page 2 of 6
 Treatment with antihistamines should be administered
w/care since these drugs are excreted in breast milk.
o Intranasal corticosteroids are safe and without teratogenic
o Immunotherapyshould be AVOIDED.
o Symptoms disappear after delivery.
As much as possible we don’t give steroids only anti-histamines.
D. RHINITIS IN ATHLETES
 Exercise is a potent vasoconstrictor: increase airway diameter
due to decrease nasal resistance as pulse increases
 Treatment:
o Medications should not be in the DOPPING list – and its
trace should not be found in the urine or blood after the
event.
 1stgen antihistamine (e.g.
Diphenhydramine)
 Immunotherapy causes discomfort at the
site of
 injection for a few days.
 DOPPING LIST includes the ff:
vasoconstrictors &decongestants
ephedrine/pseudoephedrinein (no longer
available in the Philippines because it is used in
making shabu) phenylpropanolamine systemic
corticosteroid (e.g. Prednisone,
Methylprednisolone, Dexamethasone). Take
note of the dopping list. This came out of the quiz.
o Prescribed medicines should not alter sports performance:
 2nd generation antihistamines
 intranasal corticosteroid sprays (Drug of Choice
for all ages- children, elderly and pregnant
women)
Exercise itself improves the airway. So don’t give them anti-
histamines or steroids during marathons because it is not allowed.
RHINITIS MEDICA MENTOSA
 Occurs as a side effect from long-term use of decongestant
nasal drops, anti-HPN drugs like rauwolfia alkaloids, beta
blockers, ACEI, and oral contraceptives due to estrogen’s
vasoactive effect.
 Clinical symptoms include obstructed nasal breathing, dry
mucosa and occasional olfactory disturbances.
PROBST
Nasal hyperreactivity
 Bronchial hyperreactivity
 Heaightened activity of the nasal mucosa due to irritants
 SYMPTOMS: inflammation, disturbances in ANS
ALLERGIC RHINITIS
 Symptomatic disorder of the nose after allergen exposure by an
IgE-mediated inflammation of the nasal membranes.
 Characterized by sneezing, rhinorrhea, nasal obstruction,
conjunctival, nasal and pharyngeal itching, lacrimation.
 Seasonal in presentation (airborne pollen) or can be perennial
is there is chronic exposure to allergen.
 Occurs in atopic individuals (with family history of allergies)
who may also have eczematous dermatitis, urticaria and
With <3, TQ
asthma. 50% of the children will be affected if either parent has
allergic rhinitis
 The ability of the allergens to cause rhinitis and NOT lower
respiratory tract infection is due to their huge size, 10 to 100
μm and retention within the nose.
 Prevalence: 10-25% world’s population, affected.
Boies: Allergic rhinitis typically begins at an early age with symptoms of nasal
congestion or obstruction, sneezing, watering and itching of eyes, and
postnasal drip. Nasal polyps and sinusitis appear to be increased in subjects
with allergic rhinitis
Pathophysiology of Allergic Rhinitis
 The nose adjusts temperature and moisture of inhaled air and
filters out particulate materials >10 μm in size.
 If pollen is trapped in nasal mucosa, its outer coat is digested by
lysozymes and therefore, pollen allergens are released.
 Pollen allergens interact with intraepithelial mast cells. Later on,
eosinophils, basophils and neutrophils will also invade the nasal
mucosa.
 The mucosal surface also contains IgA and IgE. IgE fixes to the
mucosal and submucosal mast cells w/c can signal release of
histamine, LTs and PGD2, thereby causing tissue edema.
Boies: Allergic rhinitis is thought to involve reaginic antibodies, basophils,
mast cells, and the release of such mediating substances as histamine,
prostaglandin, and leukotrienes which in turn act on the nasal passages to
produce the clinical manifestations.
Note 2014B: Pathophysiologyof allergic rhinitis with site of action of
drugs. Antihistamine stops allergy symptoms by interfering with
binding of histamine. Steroids act by inhibiting gene transcription of
several proteins (IL3&4,etc) involved in the cascade of inflammation.
Best for allergies is corticosteroids but you should be careful in using
it because of the side effects.
Diagnosis of Allergic Rhinitis
 HISTORY
o Dx is mainly based here
o Patients have the same signs and symptoms
o The presence of secondary complications will make the
presentation different
 PE
o Will not tell much since all forms of rhinitis appear to have
the same symptoms
o Rhinoscopy / Nasal Endoscopy
Page 3 of 6
  Nasal turbinates will appear pale blue, gray, dull
red, or red.
 Nasal discharge is minimal to profuse, watery to
mucoid
 Mucus threads
Boies: Physical examination in the subjects with allergic rhinitis will reveal
excessive lacrimation and reddening of the schlera and conjunctiva,
periorbital darkness, moderate to marked swelling of nasal turbinates, which
will be pale to purplish in color, clear thin nasal secretions, and a lateral
crease of the ridge of the nose.

 IMAGING TECHNIQUES
o Mainly done to R/O infection or anatomic variations in the
osteomeatal complex (ex. XRAY, CT Scan of the paranasal
sinuses)
Boies: Bilateral involvement is more compatible with an allergic mechanism
then is unilateral disease. If you are in mild to moderate persistent allergic rhinitis you use
Globally Important Allergens
 SKIN PRICK TEST  House dust mite – multiplies faster in air-conditioned rooms.
o Only diagnostic tool for allergic rhinitis People are not allergic to mites of dust but to dung!
o Done to check for the specific allergen causing rhinitis  Pets
o Not done for all patients due to high cost  Cockroaches
o Indications:  Diesel exhaust
 Unresponsive patients to pharmacotherapy  Ozone
 Patients with multiple organ involvement  Tobacco, smoke -
 Patients for hyposensitization  Grass, trees,
Boies: Dietary test (provocative food test and various elimination diets),  Molds
cytotoxic food test (leukocytes from the buffy coat of the patient’s plasma
are destroyed in the presence of food antigen) Radioallergosorbercy test Egyptian Theory of the Nose
(measure the concentration of IgE in patient’s antibodies with specific
- Once air enters the nose, it goes to the heart and exits the
concentrations of antigen coupled with radioactive paper)
rectum.
- They used MYRRH with dung of white dogs as
Classification of Allergic Rhinitis decongestants. First to use nasal decongestants

OLD CLASSIFICATION
Epidemiology
1. Seasonal – esp. pollen season (Hay fever- Probst)
 Prevalence varies from 0.8 and 14.95% in 6-7 year olds and
2. Perennial – throughout the year (Presence of Allergen in
between 1.4 and 39.7% in 13-14 year olds.
the environment- Probst)
 Increase in age also increases risk for allergic rhinitis BUT
3. Occupational - (Latex- Probst)
people who are ≥ 65 years gave decreased prevalence
 Low prevalence in Indonesia, Greece, Quatar, Bahrain and
 Based on severity and is subdivided into mild or moderate-
deserts (the sand does not have allergens!)
severe, depending on the symptoms and quality of life
 Increase prevalence in Australia, UK and USA.
 Also based on duration and is subdivided into intermittent
 Avoidance of allergens is the ultimate therapy for allergic
or persistent.
rhinitis.
NEW CLASSIFICATION according to ARIA  Once you have it, you have it for life!
 40-50% of patients with allergic rhinitis have asthma
 Based on severity and is subdivided into mild or moderate-
 Rhinitis occurs in > 75% of allergic asthmatics
severe, depending on the symptoms and quality of life
 Also based on duration and is subdivided into intermittent
or persistent. CLINICAL CLASSIFICATION OF ALLERGIC RHINITIS

We do not treat the allergy but the symptoms. SNEEZERS and RUNNERS
- Paroxysmal sneezing
- Watery rhinorrhea
(anterior more than
posterior)
- Itchy nose
- Nasal blockade
- Diurnal variation (worse
during the day)
- Associated with
conjunctivitis
BLOCKERS
- Little or no sneezing
- Thick nasal mucus (more
posterior than anterior)
- No itchy nose
- Severe nasal blockade
- Constant day and night but
may worsen during the
night
- Cannot go to sleep

With <3, TQ Page 4 of 6

 Treatment
 Avoid allergens – FIRST AND BEST TREATMENT
 Particular allergens:
o House mites
 Wash beddings weekly at 60C
 Encase pillow and mattress in allergen
impermeable covers
 Dispose feather beddings
 Avoid using cotton pillows and comforters made
of goose feathers (hyperallergenic).
 Use vacuum cleaner with HEPA filter
 Replace carpets with linoleum or wooden floors
 Remove curtains, pets and soft toys from
bedroom
 Provide adequate ventilation and decrease
humidity
o Pollens
 Remain indoors at peak pollen times
 Wear sunglasses and masks
 Use air-conditioning if possible
 Install car pollen filters
Boies: make proper alterations in environment such as preventing
unnecessary exposure, air conditioning of car and home as well as
utilization of air filters. [Boies]
o Pets
Exclude pets from bedrooms and if possible from
homes
o Cockroaches – ERADICATE!
o Molds
 Use humidifier
 Ensure dry housing
 Use ammonia to remove mould from bathrooms
and other wet spaces in the house
Boies: Avoid sleeping in damp areas, windows should be closed at
night.
In Summary (AFP 2010 Guidelines)
With <3, TQ
 For specific conditions:
A. MILD ALLERGIC RHINITIS
- Oral anitihistamine or antihistamine-decongestant
combination. H1-receptor antagonists (eg.
Diphenhydramine, Loratidine) that are useful in
treating allergic rhinitis but of little effect if rhinitis is
associated with colds.
- Intranasal cromolyn solution. Works almost 100% of
the time. This has anti-inflammatory activity,
administered by aerosol spray or nebulizer.
Boies: Chromolyn sodium decrease the release of mediating substances.
It is considered a preventive medication that is given before the onset
of symptoms.
B. MODERATE ALLERGIC RHINITIS
- Intranasal corticosteroids
- Antihistamine-decongestant combination
- Immunotherapy if symptoms persist for 2-3 months.
C. SEVERE ALLERGIC RHINITIS
- Intranasal corticosteroids
- Antihistamine-decongestant combination
- Oral corticosteroids – short term use of Prednisone is
okay but long term use of prednisolone is NOT.
- Immunotherapy if rhinitis is persistent. This is
expensive
Allergic Rhinitis (PROBST)
SYMPTOMS: obstructed nasal breathing, sneezing attacks, watery
nasal discharge, itching of the nose and eyes (conjunctivitis)
DIAGNOSIS: detailed allergy history; bluish-purple discoloration of
the mucosa-seasonal allergic rhinitis; bright red and inflammatory
changes- perenial.
TREATMENT: BEST IS TO AVOID ALLERGEN (See Table on p.52 for
medications)
Long term treatment
 Immunotherapy/ hyposensitization therapy
 Surgical treatment- MAIN GOAL: reduce the size of turbinates
by coagulation (turbinate cautery), laser
Pharmacotherapy
2nd Generation Antihistamines (GOLD STD)
 Potent noncompetitive H1 receptor antagonists
 Rapid onset and 24 hour duration of action
 LESS sedation
 LESS cardiac toxicity
 NO interference in activity by food
 Examples
- Cetirizine
- Ebastine
- Fexofenadine
- Loratidine
- Mizolastine
- Acrivastine
- Azelastine
Boies: Since patient exhibit marked variability in response to various
antihistamines, individualization of doses and frequency administration is
important.
Intranasal Corticosteroids
 Fluticasone and Mometasone are mainstay drugs because
they have decreased bioavailability (BA) so they have less
systemic effects. They only stay in the mucosa lining.
Page 5 of 6
  Flunisolide(20% BA), Beclomethasone. Budesonide (11%
BA), Triamcinolone, have increased BA so they have more
systemic effects (more side effects)
Avamys (Fluticasone furoate) is now being used.
Boies: Allergen injection, immunotherapy of hyposensitization is done when
more conservative measures are not successful. Allergen injection with
gradually increasing doses of the causative allergen to induce tolerance to
them in the allergic subjects.
Most effective treatment is still water therapy with nasal spray and
nasal douche
OTHERS
Normal Physiology
 Ciliary action propels mucus towards the back of the nose so
you singhot and then lunok.
 You can blow your nose but DO NOT do it excessively because
you cannot eliminate all the mucus anteriorly. JUST SWALLOW
THE MUCUS via POSTERIOR ROUTE!
 Do not blow your nose because it will counterflow the ciliary
movement (ant-post) of the ciliary mucosa therefore destroying
the mechanism.
 Sneezing is a means to spread the disease.
 If you have asthma you will have rhinitis, if you have asthma
then you have rhinitis because of the universal airway.
Addtional Info from Probst (NOT DISCUSSED IN THE LECTURE)
A. Wegener Granulomatosis
 Granulomatous disease that starts with formation of primary
granulomas in the connective tissue that progresses to
vascular involvemnet in the form of necrotizing vasculits
 Lesions usually develop in the head and neck but nose is the
predominant site. May also develop in trachea and middle ear.
 SYMTPOMS Nasal airway obstruction, bloody nasal discharge,
severe crusting in the nasal cavity and nasopharynx
B. Specific Chronic Rhinitis (p.51)
1. Tuberculosis
 Primary infection: Nasal mucosa forming primary complex 6
weeks after infection
 Lupus Vulgaris: most common post-primary form of
cutaneous tuberculosis. Destruction of nasal structure from
the inside.
2. Sarcoidosis
 Common granulomatous systemic disease of unknown etiology
 Woman under 40
 Nasal symptoms as initial manifestation
 Lupus Pernio- external nose characteristic skin changes that
resemble chill blains (are small, itchy, painful lumps that
develop on the skin. They develop as an abnormal response to
cold- internet)(pernio)
 Yellowish submucosa nodules that have gross appearance of
intramucosal granulomas
3. Rhinoscleroderma
 Most common etio agent: Klebsilla Pneumonia
 Features atrophic rhinitis- fetid nasal discharge, dry mucosa
and crusting
With <3, TQ
4. Actinomycosis
 Gram (+)- Actinomyces israelli -immunocompromised patients
 Uncommon symptomatic nose and PNS
 Left untreated will cause tissue destruction or worst fatal
outcome
5. Syphillis
 Tertiary stage: nasal involvement
 Appearance of isolated gummata/ diffused gummatus
infiltration of the nasal cavity
6. Malleus
 Rare infectious disease (Psedommonas mallei)
 Transmitted to human from horses or house pets
 SYMPTOMS: inflammatory swelling, pustule formation,
ulceration with viscous nasal discharge
7. Fungal Infections
a. Aspergillosis- most common fungal colonization occuring in the
PNS
b. Mucomycosis- resembles aspergillosis, mainly affects
immunocompromised patients
c. Rhinosporidiosis- very rare and caused by Rhinosporidium seebei
C. Vasomotor Rhinitis
 Resembles allergic rhinitis but NO EVIDENCE that the patient
has been previously sensitized
 Pathogenesis: involve neurovascular autonomic disturbances
in regulating the tonus of the nasal mucosal vessels
 Symptoms: obstructed nasal breathing, watery nasal discharge,
sneezing
 History: temp change, consumption of hot and cold liquid
 Emotional stress
 Inspection: same appearanec as allergic rhinitis
 TREATMENT: antihistamins, corticosteriod nasal spray, Kneipp
system therapy- ice water is sniff up the nose as way of
“training” the neuroautonomic regulation of the blood supply
of the nasal mucosa; surgical reduction of turbinates especially
pronounced inferior turbinate hyperplasia
D. Atrophic Rhinitis
 Same presentation as Rhinosclerema
 SYMPTOMS: dryness of nasal mucosa
 Severe: secondary to bacterial colonization marked by fetid
nasal odor which is not perceived by the patient d/t
degenerating olfactory epithelium
 Etiology unknown
 Endoscopic examination: broad nasal cavity lined w/ dry,
crusted mucosa
 TREATMENT: conservative, do not use decongestant nasal
drops
TRIVIA!
You say GOD BLESS YOU to people who sneeze because we adopted that
from Pope Gregory 1. During his time, the Bubonic and Pneumonic plagues
were causing widespread deaths and it was common knowledge at that time
that once you sneeze, it was almost certain that you have the disease ---
therefore you were bound to die (So parang FINAL BLESSING).
REMINDERS:
-read on Aspirin Induced Rhinitis (Can’t find it in Probst. Sinabi nya sa
recording. And his recording is puro NEXT SLIDE, ALAM NYO NA YAN.
MARATHON. Hay.)
SOURCES: 2013A Trans, 2014A & B, Probst, Boies ,Recording 2013 lecture
Page 6 of 6