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Lecture topics
- The upper-airway framework
- Two initiating pathways can converge
- Extension beyond the nasal cavity
- Lymphocytes in chronic rhinitis
- The polyp contains loose edematous stroma
- Rhinitis commonly precedes sinusitis
- Inherited ciliary dysfunction is another cause
- Teaching synthesis
Slide index & full transcript (67 slides)
Text from the original slides, in presentation order. Diagrams and images remain in the viewer above.
Slide 1 · Chronic rhinitis
Recurrent nasal inflammation, mucosal injury, and impaired secretion drainage
Dr Abu Suraih Sakhri
MBBS, MD (Pathology)
www.abusuraihsakhri.com
Slide 2 · Learning objectives
Trace repeated microbial or allergic attacks to chronic rhinitis and bacterial superinfection.
Identify epithelial injury and the three inflammatory cell types described in the source.
Connect nasal obstruction with polyps, impaired drainage, and sinusitis.
Slide 3 · The upper-airway framework
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
The upper airway includes the nose, pharynx, and larynx.
Nasal inflammation is an important group of upper-airway disorders.
The nose and accessory sinuses share interconnected drainage pathways.
Slide 4 · Infectious, allergic, and chronic processes
Microbial rhinitis
Allergic rhinitis
Repeated mucosal inflammation
Slide 5 · Chronic rhinitis: The defining sequence
Repeated microbial or allergic rhinitis provides the antecedent history.
Superimposed bacterial infection can complicate the recurrent process.
The mucosa develops surface injury and an inflammatory-cell infiltrate.
Slide 6 · A recurrent process differs from one cold
Acute episode
Acute infectious rhinitis often clears rapidly.
Chronic process
Chronic rhinitis follows repeated episodes of inflammation.
Time course and preceding episodes alter clinicopathologic interpretation.
Slide 7 · Distinct starting mechanisms
Allergic
Allergen exposure initiates an IgE-mediated mucosal reaction.
Microbial
Viral respiratory infection initiates microbial rhinitis.
Both pathways can recur and precede chronic inflammation.
Slide 8 · Allergic rhinitis: Common triggers
Relevant allergens include plant pollens, fungi, animal allergens, and dust mites.
The inflammatory process is an IgE-mediated hypersensitivity reaction.
Early and late phases occur in the accompanying immune response.
Slide 9 · Allergic mucosal response
Allergen exposure
IgE-mediated immune response
Edema, mucus secretion, eosinophils
Slide 10 · Infectious rhinitis: Acute mucosal effects
Rhinoviruses, echoviruses, and adenoviruses are described as viral causes.
Acute mucosal edema and thickening narrow the nasal cavity.
Secondary bacterial infection can produce mucopurulent or suppurative exudate.
Slide 11 · Two initiating pathways can converge
Repeated microbial rhinitis
Repeated allergic rhinitis
Inflamed nasal mucosa
Slide 12 · Superimposed bacterial infection
Bacterial superinfection is explicitly described in the course of chronic rhinitis.
This process adds infection to an already repeatedly inflamed mucosa.
An allergic episode alone must not be equated with bacterial infection.
Slide 13 · Core pathogenic sequence
Recurrent episodes
Bacterial superinfection
Mucosal inflammatory injury
Slide 14 · Drainage modifies disease progression
Septal deviation or polyps
Impaired secretion drainage
Greater microbial susceptibility
Slide 15 · Septal deviation is a structural risk
Schematic — not a clinical or histologic specimen
An altered septal contour can impede normal secretion drainage.
The key effect is impaired passage of nasal secretions.
Poor clearance predisposes the mucosa to microbial invasion.
Slide 16 · Nasal polyps provide a second obstruction
Schematic — not a clinical or histologic specimen
Recurrent rhinitis may produce focal mucosal protrusions.
When large or multiple, polyps may encroach on the airway.
Polyp-associated obstruction can impede sinus drainage.
Slide 17 · Obstructions share a functional consequence
Deviated nasal septum
Mucosal polyps
Impaired drainage of secretions
Slide 18 · The inflammation–obstruction relationship
Repeated mucosal inflammation
Nasal obstruction or swelling
Reduced secretion drainage
Slide 19 · Extension beyond the nasal cavity
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
Infection associated with chronic rhinitis may spread into sinuses.
Nasal and sinus spaces communicate through drainage routes.
Rhinitis and sinusitis therefore can form a connected disease process.
Slide 20 · Integrated pathogenesis
Repeated inflammation
Mucosal injury
Impaired drainage
Bacterial superinfection
Possible sinusitis
Slide 21 · Histology has two complementary compartments
Schematic — not a clinical or histologic specimen
Inspect the mucosal surface for epithelial integrity or loss.
Inspect the underlying tissue for inflammatory-cell infiltrates.
The stated inflammatory response includes neutrophils, lymphocytes and plasma cells.
Slide 22 · Superficial epithelial desquamation
Schematic — not a clinical or histologic specimen
Desquamation refers to shedding or loss of the lining epithelial cells.
Superficial mucosal injury is a common change in chronic rhinitis.
Evaluate epithelial changes separately from inflammatory-cell composition.
Slide 23 · Superficial mucosal ulceration
Schematic — not a clinical or histologic specimen
Ulceration produces a defect in the mucosal surface.
The source permits superficial mucosal ulceration in chronic rhinitis.
Surface ulceration is not equivalent to an intact reactive epithelium.
Slide 24 · Intact and injured mucosal surfaces
Intact surface
The intact surface maintains a continuous epithelial lining.
Injured surface
An injured surface may demonstrate desquamation or ulceration.
The adjacent inflammatory infiltrate helps characterize the process.
Slide 25 · Chronic rhinitis contains a mixed infiltrate
Neutrophil
Lymphocyte
Plasma cell
Schematic — not a clinical or histologic specimen
Variable neutrophils may be present.
Lymphocytes are also described in the inflammatory infiltrate.
Plasma cells complete the listed chronic-rhinitis cell spectrum.
Slide 26 · Neutrophils in chronic rhinitis
Neutrophil
Lymphocyte
Plasma cell
Schematic — not a clinical or histologic specimen
Neutrophils are one component of the mixed inflammatory response.
Their proportion may vary across lesions.
Neutrophils alone do not establish a single specific cause.
Slide 27 · Lymphocytes in chronic rhinitis
Neutrophil
Lymphocyte
Plasma cell
Schematic — not a clinical or histologic specimen
Lymphocytes can infiltrate the mucosa in chronic rhinitis.
They coexist with other cell types in the source description.
Interpret them alongside epithelial injury and clinical context.
Slide 28 · Plasma cells in chronic rhinitis
Neutrophil
Lymphocyte
Plasma cell
Schematic — not a clinical or histologic specimen
Plasma cells are named in the source inflammatory-cell spectrum.
Relative abundance varies within this mixed infiltrate.
No numerical plasma-cell threshold is supplied for this entity.
Slide 29 · The inflammatory mixture is variable
Neutrophils
A lesion may show a conspicuous neutrophil component.
Mononuclear cells
Another lesion may contain more lymphocytes and plasma cells.
There is no mandatory fixed ratio among these three populations.
Slide 30 · Allergic and chronic patterns are distinct
Allergic rhinitis
Allergic rhinitis has an eosinophil-rich infiltrate in the neighboring text.
Chronic rhinitis
Chronic rhinitis includes variable neutrophils, lymphocytes, and plasma cells.
Do not require eosinophilia in every chronic-rhinitis specimen.
Slide 31 · Edema contributes to tissue and airway change
Schematic — not a clinical or histologic specimen
Allergic mucosal reactions can produce edema and mucus secretion.
Nasal-polyps stroma may be markedly edematous.
Swelling and protrusions can reduce available airway and drainage space.
Slide 32 · A structured mucosal review
Surface epithelium
Stromal edema and architecture
Inflammatory cell populations
Slide 33 · Morphology synthesis: Chronic rhinitis
Superficial epithelial desquamation or ulceration is typical.
Neutrophils, lymphocytes, and plasma cells occur in variable proportions.
Interpret these findings in recurrent inflammation with possible superinfection.
Slide 34 · How polyps arise from recurrent rhinitis
Schematic — not a clinical or histologic specimen
Repeated rhinitis can produce focal protrusions of mucosal tissue.
A polyp is a localized expansion rather than diffuse flat mucosal swelling.
Its significance increases when it impairs the airway or drainage.
Slide 35 · Polyp size and encroachment
Schematic — not a clinical or histologic specimen
Nasal polyps may attain lengths of 3–4 cm.
Large or multiple lesions can encroach on the airway.
Sinus drainage can be disrupted by extensive polyposis.
Slide 36 · The polyp contains loose edematous stroma
Schematic — not a clinical or histologic specimen
The polyp core is edematous mucosa with loose stromal architecture.
The expanded stroma forms the substance of the mucosal protrusion.
This is inflammatory polyp architecture, not tumor staging.
Slide 37 · Glandular changes within nasal polyps
Schematic — not a clinical or histologic specimen
Hyperplastic mucus glands can be identified.
Cystic gland changes are another described finding.
These glands coexist with stromal edema and inflammation.
Slide 38 · Polyps have their own cell spectrum
Neutrophil
Eosinophil
Plasma cell
Schematic — not a clinical or histologic specimen
Polyp infiltrates can contain neutrophils.
Eosinophils are often important in the described inflammatory mixture.
Plasma cells are also listed in the adjacent pathology description.
Slide 39 · Polyp surface: Intact versus ulcerated
Intact surface
Without bacterial infection the polyp surface may remain intact.
Ulcerated surface
With infection the mucosal surface may become ulcerated.
Surface integrity helps interpret superimposed inflammation.
Slide 40 · A polyp does not always signify atopy
Most people with nasal polyps are not atopic discussion.
An eosinophil-rich polyp does not independently establish systemic atopy.
Interpret morphology together with clinical inflammatory context.
Slide 41 · Polyps link chronic inflammation to obstruction
Recurrent nasal inflammation
Polypoid mucosal expansion
Obstructed airway and sinus drainage
Slide 42 · Compare three related nasal entities
Process
Characteristic morphology
Functional effect
Infectious rhinitis
Acute swollen mucosa, catarrh
Possible bacterial exudate
Chronic rhinitis
Epithelial injury, mixed infiltrate
Repeated inflammation and superinfection
Inflammatory polyp
Edematous protruding mucosa, glands
Potential airway and outflow obstruction
Slide 43 · The nasal–sinus relationship
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
Chronic nasal infection can extend into the sinuses.
Rhinitis often precedes acute sinusitis.
Edema and obstruction connect nasal and sinus inflammation.
Slide 44 · Rhinitis commonly precedes sinusitis
Rhinitis
Mucosal edema
Impaired sinus outflow
Slide 45 · An alternative origin: Dental infection
Rhinitis route
Most acute sinusitis cases are preceded by rhinitis.
Odontogenic route
A periapical infection may extend through the maxillary sinus floor.
These represent different anatomic routes into sinus inflammation.
Slide 46 · Outflow obstruction retains sinus contents
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
An inflamed sinus develops edematous mucosa.
Edema obstructs drainage from the cavity.
Trapped secretions can accumulate behind the narrowing.
Slide 47 · Empyema develops in an infected sinus
Mucosal inflammation
Impaired outflow
Purulent retention: Empyema
Slide 48 · Mucocele and empyema are distinct
Mucocele
A mucocele results from accumulation of retained mucus.
Empyema
Empyema involves purulent material retained in an infected sinus.
Both implicate impaired drainage, but the contents differ.
Slide 49 · Anatomic sites of outflow obstruction
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
Frontal sinus drainage is most often affected in the source account.
Anterior ethmoid outflow obstruction is another less common site.
These blockages can permit abnormal accumulation of secretions.
Slide 50 · Acute sinusitis can progress to chronic disease
Acute sinusitis
Persistent drainage impairment
Chronic sinusitis
Slide 51 · Polymicrobial chronic sinusitis
Most chronic sinus infections in the source are polymicrobial.
Microbes often include members of the normal oral microbial community.
This is different from assuming a single named pathogen in every patient.
Slide 52 · Inherited ciliary dysfunction is another cause
Impaired ciliary action
Poor mucociliary clearance
Sinusitis in Kartagener syndrome
Slide 53 · Kartagener syndrome: Associated features
Sinusitis can be an uncommon manifestation of Kartagener syndrome.
Bronchiectasis is also part of the described syndrome.
Situs inversus occurs in the classic syndromic constellation.
Slide 54 · Severe fungal sinus infection
Fungal causes can produce severe chronic sinus infection.
Mucormycosis is specifically highlighted in the source.
Diabetes is a relevant predisposing clinical context.
Slide 55 · Spread from sinus to the orbit
Sinus cavity
Nasal space
Schematic — not a clinical or histologic specimen
Sinus infection can occasionally extend into the orbital region.
This represents extension beyond the local mucosal compartment.
Orbital spread is a serious but uncommon consequence.
Slide 56 · Spread into bone: Osteomyelitis
Sinus infection
Extension through adjacent bone
Osteomyelitis
Slide 57 · Intracranial venous complication
Severe sinus infection
Extension into cranial vault
Septic dural venous thrombophlebitis
Slide 58 · Complications follow a severity hierarchy
Localized mucosal sinusitis
Obstruction and retained contents
Occasional orbital, bone, or intracranial spread
Slide 59 · Case 1: Septal obstruction
A patient experiences repeated inflammatory episodes of rhinitis.
A deviated septum impedes the normal flow of secretions.
Question: Which functional change increases microbial susceptibility?
Slide 60 · Case 1: The relevant intermediate step
Deviated septum
Impaired secretion drainage
Increased likelihood of invasion
Slide 61 · Case 2: A nasal mucosal specimen
Histology shows superficial desquamation of nasal epithelium.
Neutrophils, lymphocytes and plasma cells are found in the mucosa.
Question: Which elements match the chronic-rhinitis description?
Slide 62 · Case 2: Morphological interpretation
Schematic — not a clinical or histologic specimen
Surface epithelial injury corresponds to desquamation or ulceration.
The infiltrate matches the described variable inflammatory-cell mixture.
These findings alone do not identify an individual organism.
Slide 63 · Case 3: Obstruction by nasal polyps
Repeated rhinitis is followed by formation of multiple large polyps.
The sinus outflow tract becomes obstructed.
Question: What two different types of sinus retention may occur?
Slide 64 · Case 3: Retained mucus versus pus
Mucocele
Mucocele denotes mucus accumulation behind obstruction.
Empyema
Empyema denotes accumulation of purulent material.
Both connect to impaired outflow but describe different contents.
Slide 65 · Unified clinicopathologic model
Repeated microbial or allergic rhinitis
Mucosal injury
Polyps or septal obstruction
Impaired drainage
Sinus extension may occur
Slide 66 · Teaching synthesis
Repeated microbial or allergic rhinitis can precede chronic mucosal inflammation.
The principal histologic findings are epithelial injury and a mixed cellular infiltrate.
Drainage impairment links nasal disease to bacterial infection and sinusitis.
Slide 67 · References
Robbins, Cotran & Kumar. Pathologic Basis of Disease. Eleventh edition. Elsevier, 2026.
Relevant contiguous sections: Infectious Rhinitis; Allergic Rhinitis; Nasal Polyps; Chronic Rhinitis; Sinusitis.