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/  Paradoxically, exposure to dogs, cats and endotoxin early in
preservatives childhood will decrease risk of allergic sensitization.
D. Rhinitis Associated with Emotional States  Treatment:
 Anxiety, conflict, frustration, resentment, recollection o Children with severe and persistent symptoms are given
of humiliating and frustrating experiences intranasal glucocorticoids (e.g. budesonide, mometasone,
Boies: Fear and dejection results in shrinkage and pallor of the nasal mucosa fluticasone) because they offer greater topical activity
while anxiety, conflict, frustration, and resentment result in hyperemia, with lower systemic exposure and a better safety profile.
swelling and hypersecretion. o Mometasoneis approved for >2 years old
E. Occupational Rhinitis o Fluticasone is approved for >4 years old
 Airborne agents present in the workplace such as o Budesonide is approved for >6 years old
those in the laboratory (e.g. animals), grains, wood o Do NOT give intramuscular & oral steroids!!!
dust, latex, and chemicals. o Do NOT give topical vasoconstrictors because they have a
F. Hormonal Rhinitis narrow margin of toxicity and therapeutic dose!!!
 During the 3rd trimester of pregnancy = status and  Drixin (oxymetazoline) is a decongestant and
well-being of both the mother and baby should be vasoconstrictor whichadults can use for a
taken into account during management. maximum period of 1 week. Using it for >1 week
 Puberty will cause rebound phenomenon.
 Hypothyroidism  [Nelson] excessive use of Oxymetazoline in
 Acromegaly children can cause profound neurologic
depression and using it for >3 days will cause
Boies: Estrogen stimulate vascular congestion of the nasal membranes. SEVERE rebound nasal congestion. Children who
During pregnancy, as the levels of estrogen rise, symptoms of nasal
are >6 years old can use oxymetazoline 0.05% 2-
congestion usually begin during the fourth to fifth month and progress to
term, paralleling the increased production of estrogen. Hypothyroidism could 3 drops or 1-2 metered sprays 2x/day.
also cause nasal obstruction and relief can be obtained with the use of o Do NOT give SEDATING FIRST GENERATION
thyroid extract. ANTIHISTAMINES and LORATIDINE!!!
 Second generation antihistamines are the drugs
G. Drug-induced Rhinitis of choice because they cause less sedation.
 Topical ophthalmic agents (beta blockers in glaucoma)
 Aspirin for CVS problems ALWAYS REMEMBE! Allergic rhinitis is Ig-E mediated. A child is not
 Inhibit the COX pathway and shifts arachidonic acid born with rhinitis. Usually nasal obstruction is the reason why they
metabolism towards lipooxygenase production are brought for consult.
resulting in increase of leukotrienes, which in turn Treatment: We avoid giving steroids to children.
causes increased mucus secretion.
 NSAIDS B. RHINITIS IN THE ELDERLY
 Chlorpromazine (antipsychotic drug)  Allergy is a less common cause of rhinitis for >65 years old.
 Reserpine and ACEI (HTN)  Atrophic rhinitis is more common. This is a condition of nasal
 Viagra (BUT NOT PROVEN YET). discomfort or ‘stuffiness’. The membranes appear dry, smooth,
 Rhinitis medicamentosa (decongestants that treat shiny and with crusts. The cause is idiopathic. In severe cases,
rhinitis can also cause rhinitis) there is secondary bacterial colonization which causes a foul
odor (ozena) that the patient cannot perceive due to
TREATMENT : The most important step is to eliminate the cause by degeneration of the olfactory epithelium.
removing chronic irritants from the environment or by surgically  Decongestants, particularly older antihistamines (1st gen) may
correcting any intranasal pathology. Supportive measures such as cause GI upset, nausea, constipation or diarrhea, and other
decongestant nose drops or nasal irrigation with saline solution are anticholinergic effects such as dry mouth, blurred vision and
of only temporary benefit. urine retention.
 Treatment:
Boies: Rhinitis Medicamentosa – Results from the abuse of o Intranasal corticosteroid such as Beclomethasoneand
sympathomimetic decongestant nose drops and nasal spray. After an initial Flunisolide. These are administered as nasal sprays to
vasoconstriction, a secondary vasodilation (rebound vasodilation) occurs reduce systemic absorption and thus lower adverse effects.
which can make the nasal obstruction worse than before. o NON-sedating antihistamine (2nd gen) such as Loratidine
Other drugs that have been implicated: rauwolfia serpentinam alcohol,
(Claritin) and Cetirizine are drugs of choice.
tobacco and hashish.
o Oxymetazolineshould be avoided. At high doses,
Oxymetazoline causes clonidine-like effects such as low BP
SPECIAL PATIENTS WITH RHINITIS and low total peripheral resistance.
A. RHINITIS IN CHILDREN
C. RHINITIS IN PREGNANCY
 Allergic rhinitis is part of ‘ALLERGIC MARCH’ and progressively
gets worse  Due to hormonal changes especially during the 2nd month AOG.
This is caused by estrogen-induced swelling of the mucosa with
 Starts at 2-3 y.o.,but is fully diagnosed at 6yoor at school-age.
nasal airway obstruction.
 Infants do not have allergic rhinitis because this condition is
 Treatment:
acquired. If infants do get rhinitis, this is because of early
o Medications may cross placenta during the 2nd and 3rd
exposure to food or milk formulas.
trimesters so they are treated with topical antihistamines.

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 Treatment with antihistamines should be administered asthma. 50% of the children will be affected if either parent has
w/care since these drugs are excreted in breast milk. allergic rhinitis
o Intranasal corticosteroids are safe and without teratogenic  The ability of the allergens to cause rhinitis and NOT lower
o Immunotherapyshould be AVOIDED. respiratory tract infection is due to their huge size, 10 to 100
o Symptoms disappear after delivery. μm and retention within the nose.
 Prevalence: 10-25% world’s population, affected.
As much as possible we don’t give steroids only anti-histamines.
Boies: Allergic rhinitis typically begins at an early age with symptoms of nasal
D. RHINITIS IN ATHLETES congestion or obstruction, sneezing, watering and itching of eyes, and
postnasal drip. Nasal polyps and sinusitis appear to be increased in subjects
 Exercise is a potent vasoconstrictor: increase airway diameter
with allergic rhinitis
due to decrease nasal resistance as pulse increases
 Treatment:
Pathophysiology of Allergic Rhinitis
o Medications should not be in the DOPPING list – and its
 The nose adjusts temperature and moisture of inhaled air and
trace should not be found in the urine or blood after the
filters out particulate materials >10 μm in size.
event.
 1stgen antihistamine (e.g.  If pollen is trapped in nasal mucosa, its outer coat is digested by
Diphenhydramine) lysozymes and therefore, pollen allergens are released.
 Immunotherapy causes discomfort at the  Pollen allergens interact with intraepithelial mast cells. Later on,
site of eosinophils, basophils and neutrophils will also invade the nasal
 injection for a few days. mucosa.
 DOPPING LIST includes the ff:  The mucosal surface also contains IgA and IgE. IgE fixes to the
vasoconstrictors &decongestants mucosal and submucosal mast cells w/c can signal release of
ephedrine/pseudoephedrinein (no longer histamine, LTs and PGD2, thereby causing tissue edema.
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 Boies: Allergic rhinitis is thought to involve reaginic antibodies, basophils,
mast cells, and the release of such mediating substances as histamine,
vasoactive effect.
prostaglandin, and leukotrienes which in turn act on the nasal passages to
 Clinical symptoms include obstructed nasal breathing, dry produce the clinical manifestations.
mucosa and occasional olfactory disturbances.
Note 2014B: Pathophysiologyof allergic rhinitis with site of action of
PROBST drugs. Antihistamine stops allergy symptoms by interfering with
Nasal hyperreactivity binding of histamine. Steroids act by inhibiting gene transcription of
 Bronchial hyperreactivity several proteins (IL3&4,etc) involved in the cascade of inflammation.
 Heaightened activity of the nasal mucosa due to irritants
 SYMPTOMS: inflammation, disturbances in ANS Best for allergies is corticosteroids but you should be careful in using
it because of the side effects.

ALLERGIC RHINITIS Diagnosis of Allergic Rhinitis

 Symptomatic disorder of the nose after allergen exposure by an  HISTORY
IgE-mediated inflammation of the nasal membranes. o Dx is mainly based here
o Patients have the same signs and symptoms
 Characterized by sneezing, rhinorrhea, nasal obstruction,
o The presence of secondary complications will make the
conjunctival, nasal and pharyngeal itching, lacrimation.
presentation different
 Seasonal in presentation (airborne pollen) or can be perennial  PE
is there is chronic exposure to allergen. o Will not tell much since all forms of rhinitis appear to have
 Occurs in atopic individuals (with family history of allergies) the same symptoms
who may also have eczematous dermatitis, urticaria and o Rhinoscopy / Nasal Endoscopy

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

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 Treatment  For specific conditions:
 Avoid allergens – FIRST AND BEST TREATMENT A. MILD ALLERGIC RHINITIS
 Particular allergens: - Oral anitihistamine or antihistamine-decongestant
o House mites combination. H1-receptor antagonists (eg.
 Wash beddings weekly at 60C Diphenhydramine, Loratidine) that are useful in
 Encase pillow and mattress in allergen treating allergic rhinitis but of little effect if rhinitis is
impermeable covers associated with colds.
 Dispose feather beddings - Intranasal cromolyn solution. Works almost 100% of
 Avoid using cotton pillows and comforters made the time. This has anti-inflammatory activity,
of goose feathers (hyperallergenic). administered by aerosol spray or nebulizer.
 Use vacuum cleaner with HEPA filter Boies: Chromolyn sodium decrease the release of mediating substances.
 Replace carpets with linoleum or wooden floors It is considered a preventive medication that is given before the onset
 Remove curtains, pets and soft toys from of symptoms.
bedroom
 Provide adequate ventilation and decrease B. MODERATE ALLERGIC RHINITIS
humidity - Intranasal corticosteroids
o Pollens - Antihistamine-decongestant combination
 Remain indoors at peak pollen times - Immunotherapy if symptoms persist for 2-3 months.
 Wear sunglasses and masks
 Use air-conditioning if possible C. SEVERE ALLERGIC RHINITIS
 Install car pollen filters - Intranasal corticosteroids
- Antihistamine-decongestant combination
Boies: make proper alterations in environment such as preventing
unnecessary exposure, air conditioning of car and home as well as
- Oral corticosteroids – short term use of Prednisone is
utilization of air filters. [Boies] okay but long term use of prednisolone is NOT.
- Immunotherapy if rhinitis is persistent. This is
o Pets expensive
Exclude pets from bedrooms and if possible from Allergic Rhinitis (PROBST)
homes SYMPTOMS: obstructed nasal breathing, sneezing attacks, watery
o Cockroaches – ERADICATE! nasal discharge, itching of the nose and eyes (conjunctivitis)
o Molds DIAGNOSIS: detailed allergy history; bluish-purple discoloration of
 Use humidifier the mucosa-seasonal allergic rhinitis; bright red and inflammatory
 Ensure dry housing changes- perenial.
 Use ammonia to remove mould from bathrooms TREATMENT: BEST IS TO AVOID ALLERGEN (See Table on p.52 for
and other wet spaces in the house medications)
Boies: Avoid sleeping in damp areas, windows should be closed at Long term treatment
night.  Immunotherapy/ hyposensitization therapy
 Surgical treatment- MAIN GOAL: reduce the size of turbinates
In Summary (AFP 2010 Guidelines) 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.

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  Flunisolide(20% BA), Beclomethasone. Budesonide (11% 4. Actinomycosis
BA), Triamcinolone, have increased BA so they have more  Gram (+)- Actinomyces israelli -immunocompromised patients
systemic effects (more side effects)  Uncommon symptomatic nose and PNS
 Left untreated will cause tissue destruction or worst fatal
Avamys (Fluticasone furoate) is now being used. outcome

Boies: Allergen injection, immunotherapy of hyposensitization is done when 5. Syphillis

more conservative measures are not successful. Allergen injection with  Tertiary stage: nasal involvement
gradually increasing doses of the causative allergen to induce tolerance to
 Appearance of isolated gummata/ diffused gummatus
them in the allergic subjects.
infiltration of the nasal cavity
Most effective treatment is still water therapy with nasal spray and
6. Malleus
nasal douche
 Rare infectious disease (Psedommonas mallei)
 Transmitted to human from horses or house pets
OTHERS  SYMPTOMS: inflammatory swelling, pustule formation,
Normal Physiology ulceration with viscous nasal discharge
 Ciliary action propels mucus towards the back of the nose so
you singhot and then lunok. 7. Fungal Infections
 You can blow your nose but DO NOT do it excessively because a. Aspergillosis- most common fungal colonization occuring in the
you cannot eliminate all the mucus anteriorly. JUST SWALLOW PNS
THE MUCUS via POSTERIOR ROUTE! b. Mucomycosis- resembles aspergillosis, mainly affects
 Do not blow your nose because it will counterflow the ciliary immunocompromised patients
movement (ant-post) of the ciliary mucosa therefore destroying c. Rhinosporidiosis- very rare and caused by Rhinosporidium seebei
the mechanism.
 Sneezing is a means to spread the disease. C. Vasomotor Rhinitis
 If you have asthma you will have rhinitis, if you have asthma  Resembles allergic rhinitis but NO EVIDENCE that the patient
then you have rhinitis because of the universal airway. has been previously sensitized
 Pathogenesis: involve neurovascular autonomic disturbances
Addtional Info from Probst (NOT DISCUSSED IN THE LECTURE) in regulating the tonus of the nasal mucosal vessels
 Symptoms: obstructed nasal breathing, watery nasal discharge,
A. Wegener Granulomatosis sneezing
 History: temp change, consumption of hot and cold liquid
 Granulomatous disease that starts with formation of primary  Emotional stress
granulomas in the connective tissue that progresses to  Inspection: same appearanec as allergic rhinitis
vascular involvemnet in the form of necrotizing vasculits  TREATMENT: antihistamins, corticosteriod nasal spray, Kneipp
 Lesions usually develop in the head and neck but nose is the system therapy- ice water is sniff up the nose as way of
predominant site. May also develop in trachea and middle ear. “training” the neuroautonomic regulation of the blood supply
 SYMTPOMS Nasal airway obstruction, bloody nasal discharge, of the nasal mucosa; surgical reduction of turbinates especially
severe crusting in the nasal cavity and nasopharynx pronounced inferior turbinate hyperplasia

B. Specific Chronic Rhinitis (p.51) D. Atrophic Rhinitis

 Same presentation as Rhinosclerema
1. Tuberculosis  SYMPTOMS: dryness of nasal mucosa
 Primary infection: Nasal mucosa forming primary complex 6  Severe: secondary to bacterial colonization marked by fetid
weeks after infection nasal odor which is not perceived by the patient d/t
 Lupus Vulgaris: most common post-primary form of degenerating olfactory epithelium
cutaneous tuberculosis. Destruction of nasal structure from  Etiology unknown
the inside.  Endoscopic examination: broad nasal cavity lined w/ dry,
crusted mucosa
2. Sarcoidosis  TREATMENT: conservative, do not use decongestant nasal
 Common granulomatous systemic disease of unknown etiology drops
 Woman under 40
 Nasal symptoms as initial manifestation TRIVIA!
 Lupus Pernio- external nose characteristic skin changes that You say GOD BLESS YOU to people who sneeze because we adopted that
resemble chill blains (are small, itchy, painful lumps 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
develop on the skin. They develop as an abnormal response to
that once you sneeze, it was almost certain that you have the disease ---
cold- internet)(pernio) therefore you were bound to die (So parang FINAL BLESSING).
 Yellowish submucosa nodules that have gross appearance of
intramucosal granulomas REMINDERS:
-read on Aspirin Induced Rhinitis (Can’t find it in Probst. Sinabi nya sa
3. Rhinoscleroderma recording. And his recording is puro NEXT SLIDE, ALAM NYO NA YAN.
 Most common etio agent: Klebsilla Pneumonia MARATHON. Hay.)
 Features atrophic rhinitis- fetid nasal discharge, dry mucosa
SOURCES: 2013A Trans, 2014A & B, Probst, Boies ,Recording 2013 lecture
and crusting
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