ENT

PATHOLOGY
Assistan professor
Dr. Sazan Abdulwahab Mirza
Objectives:
1. list the infective disease of the nose: acute rhinitis, purulent rhinitis,
membranous rhinitis.
2. Describe acute and chronic sinusitis, tuberculosis, and fungal
infection.
3. Define inflammatory conditions: allergic nasal polyp, Wagner
granulomatosis.
4. Describe the pathogenesis and pathological features of the benign
neoplasms: sinonasal papilloma, and nasopharyngeal angiofibroma.
5. Describe the pathogenesis and pathological features of the malignant
neoplasms: sinonasal carcinoma, and nasopharyngeal carcinoma, and
olfactory neuroblastoma.
6. Discus diseases of the larynx: infectious and inflammatory
conditions: acute laryngitis, acute epiglottitis, chronic non-
Specific laryngitis, laryngeal nodule.
7. Discuss pathogenesis and pathological features of laryngeal benign
tumors: juvenile papillomatosis and adult papilloma.
8. Define laryngeal intra-epithelial proliferative lesions.
9. Discuss the pathogenesis and pathological feature of laryngeal
invasive carcinoma.
10. Discuss diseases of external ear: Non-neoplastic disorders SSS,
Tumors and tumorlike conditions: Keratotic lesions, Basal cell
carcinoma, Squamous cell carcinoma (SSS).
11. Discuss diseases of middle and inner ear: Non-neoplastic
disorders ,Tumors and tumorlike conditions: Paraganglioma,
Meningioma, Schwannoma (acoustic neuroma), Adenocarcinoma,
Squamous cell carcinoma.
Congenital (developmental) disorders of
the nose:

1. Choanal atresia: rare

- unilateral
- bilateral

2. Septal deviation: very common

- developmental
- traumatic
3. External deformities of the nose
- developmental
- post-traumatic
- After certain diseases (Syphilis, yaws, etc.)
1. Infective:
1. Acute rhinitis (coryza) = common cold
Viral
Highly contagious (airborne droplets)
- acute stage
- recovery stage
Secondary bacterial infection

2. Purulent rhinitis

3. Membraneous rhinitis:
- Diphtheria
- Pneumococci
- Staphyclococci
- Streptococci
 Chronic Rhinitis.
Chronic rhinitis is a sequel to repeated attacks of acute rhinitis,
whether microbial or allergic in origin, with the eventual
development of superimposed bacterial infection.
A deviated nasal septum or nasal polyps with impaired drainage of
secretions contribute to the microbial invasion.
Frequently, there is superficial desquamation or ulceration of the
mucosal epithelium and a variable inflammatory infiltrate of
neutrophils, lymphocytes, and plasma cells subjacent to the
epithelium.
These suppurative infections sometimes extend into the air sinuses.
Acute and Chronic sinusitis: purulent and non-
purulent, affecting mainly the maxillary sinus.
Secondary to obstruction of nasal passages,
especially within the middle meatal region.
Mucocele: late complication of chronic sinusitis
when sinus outlet is permanently obstructed,
with accumulation of inflammatory exudates and
mucin secreted by the hyperplastic glands (sterile
fluid), becomes increasingly viscous  enlarges
 thinning of sinus walls (pseudocyst).
 Tuberculosis

Represents an isolated upper respiratory tract

infection rather than a secondary spread from
pulmonary tuberculosis,
Usually associated with cervical
lymphadenopathy.
 Fungal sinusitis

Mycotic infection of chronically inflamed

sinuses, caused mainly by Aspergillus.
Occurs usually in debilitated, diabetic, or
immuno-suppressed patients.
Could be secondary to allergic sinusitis which
results in the formation of allergic mucin made
up of pools of mucin-containing eosinophils
numerous Charcot Leyden crystals and fungal
hyphae.
2. Inflammatory conditions:
Allergic nasal polyp
Not true neoplasms. They are associated with
inflammation and allergy. Generally, they are multiple
(bunch of grapes), and nearly always bilateral.
Microscopically:
composed of loose mucoid stroma and mucous glands
covered by respiratory epithelium which often shows
foci of squamous metaplasia. They are infiltrated by
lymphocytes, plasma cells, mast cells, neureophils and
eosinophils.
 Wegner’s Granulomatosis
A rapidly progressing systemic vasculitic condition
involving the nose, pulmonary as well as renal
systems. It causes similar symptoms and signs of
atrophic rhinitis (dryness, obstruction), but the
patient is extremely ill and toxic with high fever.
Microscopically:
A leukocytoplastic vasculitis with geographic
necrosis surrounded by palisaded histiocytes,
lymphocyte-poor granulomatous reaction and
epithelial ulceration.
 Wegner’s granulomatosis

DDx:
Tuberculosis.
malignant lymphoma Non hodjkan

cocaine induced lesion

immune mediated disease (SLE)
3. Benign neoplasms

A. Sinonasal papilloma
Benign neoplasm
presents in adult men with unilateral nasal
stuffiness, obstruction, and epistaxis.
Microscopically:
Proliferating columnar and/or squamous
epithelium admixed with mucin-containing cells,
Papillomas arising in the nasal septum are
usually exophytic and mushroom shaped.
These arising in the middle or inferior turbinate
or middle meatus are usually of the inverted type
with inward growth of the epithelium into the
stroma
B. Nasopharyngeal angiofibroma

It occurs almost exclusively in males. It is

androgen dependent.
It presents as polypoidal mass that bleeds
severely on manipulation.
 Nasopharyngeal angiofibroma
Microscopically:
Composed of matrix of blood vessels and fibrous tissue
stroma which may be loose and edematous or dense
acellular and highly collagenized.
The vessels range from capillary size which are
particularly common at the growing edge of the tumor,
they have got plump endothelial cells.
Larger venous size vessels are located at the base of the
lesion
4. Malignant neoplasms
Sinonasal carcinoma
unusual tumors which are often diagnosed late in
their course because of their extension to other
parts of face and skulls.
Microscopically:
Squmaous cell carcinoma, transitional cell
carcinoma, adenocarcinoma, small cell
neuroendocrine carcinoma or anaplastic
carcinoma.
 Nasopharyngeal carcinoma
Is a common leading cause of death especially
in southeast Asia and northern Africa.
Two peak age groups 15-25 and 60-69 years.
The tumor usually results from the combined
action of genetic predisposition, environmental
factors (EBV infection).
 Nasopharyngeal carcinoma
Tumor initiation usually requires EBV
expression, but the induction of preneoplastic
events and maintenance of tumor cell phenotype
requires critical cellular genes.
The viruses can be demonstrated in the tumor
tissue with in situ hybridization techniques,
immunohistochemical techniques and PCR.
 Nasopharyngeal carcinoma
Microscopically:
Two types:
those designated as (keratinizing) squamous cell
carcinoma do not show high association with EBV
and occur in old age groups.
Non-keratinizing carcinoma which has a high
association with EBV (more common)
Differentiated
undifferentiated
 Nasopharyngeal carcinoma
A high proportion of these tumors particularly in
the undifferentiated group is accompanied by a
prominent inflammatory infiltrate rich in
lymphocytes (non neoplastic component),
sometimes referred to as lympho-epithelioma.
Two patterns of cell growth are found:
well defined aggregates of epithelial cells surrounded
by fibrous tissue & lymphocytes.
neoplastic epithelial cells grow diffusely and are
closely intermingled with inflammatory cells
 Nasopharyngeal carcinoma
Spread and metastasis:
Extend to the paranasopharyngeal space and
from it along the perineural space of trigeminal
nerve.
Regional lymph nodes

Cytobkeratin
CD 45
T or B
CD 3 20
 Olfactory Neuroblastoma
A specific type of malignant neuro-ectodermal
tumor thought to arise from neuroepithelial
elements in the olfactory membrane which are
replaced by respiratory epithelium in adults.
Behavior:
local invasiveness
distant metastasis mainly to cervical lymph
nodes.
 Olfactory Neuroblastoma
Microscopically:
A cellular tumor composed of uniform small
cells with round nuclei, scanty cytoplasm,
indistinct nuclear membrane and a prominent
fibrillary or reticular background. Fibrovascular
stroma may separate the tumor cells into clusters.
 Lymphoid tumor

Malignant lymphoma can present as a mass in

sinonasal region or nasopharynx.
It is mainly of the non-Hodgkin’s type
exra modulay
 Larynx
 Supraglottis: extends from the tip of the epiglottis to
the true cords including aryepiglottic folds, false cords
and ventricles. Its origin is the 3rd and 4th branchial
pouches.
 Glottis: consists of true cords and their anterior
commissure. It originates from the 6th branchial pouch.
 Subglottis: The area between the lower border of true
cords and the first tracheal cartilage. It originates from
the 6th branchial pouch.
The lining epithelium varies from stratified squamous to
respiratory type.
Infections:
1. Acute laryngitis:
a. Isolated
b. Part of URT infection.

S&S:
• From slight hoarseness to complete loss of voice.
• Throat pain on talking or swallowing.
• Dry and irritative cough.
• Slight to moderate fever.
 Acute epiglottitis
It is a bacterial infection caused by Hemophilus
influenzae type B
It is a rare but lethal condition as it causes
respiratory tract obstruction due to massive
edema, especially in children.
Microscopically:
There is an intense acute inflammatory infiltrate
associated with edema
 Inflammation
Chronic non-specific laryngitis
Causes: infection, voice overuse, exposure to
chemical (tobacco or alcohol) and physical
agents.
Microscopically:
lymphocytic, plasmacytic, histiocytic infiltration.
epithelial hyperplasia
 Laryngeal cyst
It is of 2 types: saccular or ductal.
Saccular: cystic distention of the laryngeal
saccule (ventricle). It causes neonatal airway
obstruction.
Ductal: dilatation of mucous glands
 Inflammation
Tuberculosis: is usually associated with active
pulmonary disease.
Laryngeal granuloma: results from
endotracheal trauma caused by intubation.
 Laryngeal nodule
A non-inflammatory reaction to injury causing
hoarseness, seen most commonly in voice
overuse (singer nodule).
Microscopically:
Early: There is edema and proliferation of young
fibroblasts.
Late: dilated blood vessels with hyalinization of
the stroma
 Tumors
Juvenile laryngeal papillomatosis

presents in children and adolescents.

Having multiple papillary tumors on the true
cords.
It may spread to the other parts resulting in
extreme respiratory difficulty and death.
It is of viral etiology (HPV 11 and 6)
 Juvenile laryngeal papilloma
Recurrence is common.
Microscopically: There is papillary or acanthotic
growth of well differentiated squamous cells
retaining normal maturation pattern.
Koilocytosis and some degree of nuclear
atypia
 Squamous cell papilloma larynx

This multilayered benign-looking squamous

This multilayered
epithelium benign-looking
is arranged squamous
in a finger-like epithelium is
projections,
arranged in a finger-like
each having projections, connective
a core of vascularized each having a core of
tissue. Theconnective
vascularized Rt. Photo istissue.
a higher
Thepower showing
Rt. Photo the
is a higher power
squamous
showing epitheliumepithelium
the squamous cover of one of the
cover of papillae.
one of the papillae.
 Adult laryngeal papilloma

It has a male predominance,

does not spread or recur,
with viral etiology (HPV 11 & 6)
 Intraepithelial proliferative lesions
1- Keratosis with epithelial hyperplasia.

– smokers, singers, excessive voice use.

– hoarseness
– laryngoscopic examination: white thickening.
– Microscopically: hyperkeratotic epithelium with
acanthosis, no atypia.
 2- Dysplasia
It is characterized by varying degree of cellular atypia,
loss of normal maturation and loss of stratification.
Mild: nuclear abnormalities are slight and most marked
in the basal third of epithelium.
Moderate: more marked nuclear abnormalities. Changes
are marked in the lower 2 thirds/
Severe: involves more than 2 thirds with some
stratification of superficial layers.
Carcinoma in situ: Full thickness ( features of carcinoma
without invasion).
Severe Dysplasia / Carcinoma in situ
 Invasive carcinoma
– 5th decade and more
– males 96%
– smoking as risk factor + alcohol
– HPV does not play a role early but
contribute at later stages.
– Hoarseness
Tumors are divided to 4 types depending
on laryngoscopic evaluation as well as CT
and MRI imaging:

Glottic 60-65%
arise from true vocal cords.
tend to remain localized because of the
surrounding cartilaginous wall and paucity of
lymphocytes.
invade locally, less LN involvement.
Supraglottic 30-35%
involve false vocal cords and ventricles and laryngeal
surface of epiglottis.
LN metastases 40%
Transglottic: less than 5%
applied to cancers that cross the laryngeal ventricle.
LN involvement 52%.
Infraglottic: less than 5%
True cords with subglottic extension more than 1 cm and
tumors of subglottic region.
Frequent spread to trachea.
Cervical LN metastasis 15-22%
Transglottic Infraglottic Supraglottic
Grossly: protruding pink to gray mass that is
often ulcerated. Vocal cord tumors are keratotic.
Microscopically:
Squamous cell carcinoma: well, moderate,
poorly differentiated.
Papillary squamous cell carcinoma with an
exophytic pattern
Molecular genetic features:
Over-expression of p53 in 50%.
p53 mutation.
 Metastases of laryngeal tumors
Regional lymph nodes
Lungs
Thyroid gland
Jugular vein.
 Prognostic Factors
clinical stage and site:
glottic 80%
supraglottic 65%
transglottic 50%
subglottic 40%
microscopic grade
field size
lymph nodes
DNA ploidy
host reaction (Langerhan’s cells in the tumor stroma is of
favorable prognosis)
p53 over-expression
 Ears
Although disorders of the ear rarely shorten life, many impair its quality.

The most common aural disorders, in descending order of frequency, are:

(1) acute and chronic otitis (most often involving the middle ear and mastoid),
sometimes leading to a cholesteatoma;

(2) symptomatic otosclerosis;

(3) aural polyps;

(4) labyrinthitis;

(5) carcinomas, largely of the external ear;

(6) paragangliomas, found mostly in the middle ear.

 Inflammatory Lesions
Inflammations of the ear—otitis media, acute or chronic—occur mostly in
infants and children.
They usually produce a serous exudate (when viral in origin) but may become
suppurative with superimposed bacterial infection.
The most common offenders are Streptococcus pneumoniae, H. influenzae, and
Moraxella catarrhalis.[
Repeated bouts of acute otitis media with failure of resolution lead to chronic
disease.

The causative agents of chronic disease are usually Pseudomonas aeruginosa,

Staphylococcus aureus, or a fungus; sometimes, a mixed flora is the cause.

Chronic infection has the potential to perforate the eardrum, encroaching on the
ossicles or labyrinth, spreading into the mastoid spaces, and even penetrating
into the cranial vault to produce a temporal cerebritis or abscess. Otitis media in
the diabetic person, when caused by P. aeruginosa, is especially aggressive and
spreads widely (destructive necrotizing otitis media).
Cholesteatomas, associated with chronic otitis media, are not neoplasms,
nor do they always contain cholesterol. Rather, they are cystic lesions 1 to 4 cm
in diameter, lined by keratinizing squamous epithelium or metaplastic mucus-
secreting epithelium and filled with amorphous debris (derived largely from
desquamated epithelium).

Sometimes they contain spicules of cholesterol. The precise events involved in

their development are not clear, but it is proposed that chronic inflammation
and perforation of the eardrum with ingrowth of the squamous epithelium or
metaplasia of the secretory epithelial lining of the middle ear are responsible
for the formation of a squamous cell nest that becomes cystic.

A chronic inflammatory reaction surrounds the keratinous cyst. Sometimes,

the cyst ruptures, not only enhancing the inflammatory reaction, but also
inducing the formation of giant cells that enclose partially necrotic squames
and other particulate debris. These lesions, by progressive enlargement, can
erode the adjacent bone, or the surrounding soft tissue and sometimes produce
visible neck masses.
OTOSCLEROSIS. This is a dystrophic disease of labyrinth of
the temporal bone. The footplate of stapes first undergoes
fibrous replacement and is subsequently replaced by sclerotic
bone. The exact etiology is not known but the condition has
familial preponderance and autosomal dominant trait. It is
seen more commonly in young males as a cause for
sensorineural type of deafness.
 RELAPSING POLYCHONDRITIS.
This is an uncommon autoimmune disease characterised
by complete loss of glycosaminoglycans resulting in
destruction of cartilage of the ear, nose, eustachian tube,
larynx and lower respiratory tract.
Histologically, the perichondral areas show acute
inflammatory cell infiltrate and destruction and
vascularization of the cartilage. Late stage shows
lymphocytic infiltration and fibrous replacement.
 CHONDRODERMATITIS NODULARIS
CHRONICA HELICIS.
This condition involves the external ear superficially and
presents as a ‘painful nodule of the ear’.

The skin in this location is in direct contact with the cartilage

without protective subcutaneous layer. Histologically, the
nodule shows epithelial hyperplasia with degeneration of the
underlying collagen, chronic inflammatory cell infiltrate,
vascular proliferation and fibrosis.
 TUMOURS AND TUMOUR-LIKE LESIONS
Tumours and tumour-like conditions are relatively more common in the
external than the middle and inner ear.

The lesions seen in the external ear are similar to those seen in the skin e.g.
tumour-like lesions such as epidermal cyst; benign tumours like naevi and
squamous cell papilloma; and malignant tumours such as basal cell
carcinoma, squamous cell carcinoma and malignant melanoma. However,
tumours and tumour-like lesions which are specific to the ear are described
below.

These include the following: In the external ear—aural (otic) polyps and
cerumengland tumours.

In the middle ear—cholesteatoma (keratoma) and jugular paraganglioma

(glomus jugulare tumour).

In the inner ear—acoustic neuroma.

 AURAL (OTIC) POLYPS.
Aural or otic polyps are tumourlike lesions arising from the middle ear as a
complication of the chronic otitis media and project into the external auditory
canal. Histologically, they are composed of chronic inflammatory granulation
tissue and are often covered by metaplastic squamous epithelium or
pseudostratified columnar epithelium.

CERUMEN-GLAND TUMOURS.
Tumours arising from cerumen-secreting apocrine sweat glands of the
external auditory canal are cerumen-gland adenomas or cerumengland
adenocarcinomas and are counter-parts of sweat gland tumours
(hideradenoma and adenocarcinoma) of the skin discussed in Chapter 26.
Both these tumours may invade the temporal bone.
 Tumors
The large variety of epithelial and mesenchymal tumors that arise in the ear—
external, medial, internal—are rare save for basal cell or squamous cell
carcinomas of the pinna (external ear).

These carcinomas tend to occur in elderly men and are thought to be associated
with actinic radiation.

By contrast, those within the canal tend to be squamous cell carcinomas, which
occur in middle-aged to elderly women and are not associated with sun
exposure. Wherever they arise, they morphologically resemble their
counterparts in other skin locations, beginning as papules that extend and
eventually erode and invade locally.

Neither the basal cell nor the squamous cell lesions of the pinna commonly
extend beyond local invasion, but squamous cell carcinomas arising in the
external canal may invade the cranial cavity or metastasize to regional nodes
and, indeed, account for a 5-year mortality of about 50%.
 JUGULAR PARAGANGLIOMA (GLOMUS JUGULARE
TUMOUR, NON-CHROMAFFIN PARAGANGLIOMA).

Tumours originating from parasympathetic ganglia are called

‘paraganglioma’ and are named according to the location of the
tissue of origin. The one arising from glomus jugulare bodies of
the middle ear (jugulotympanic bodies) is called jugular
paraganglioma or chemodectoma or nonchromaffin
paraganglioma and is the most common benign tumour of the
middle ear. Histologically similar tumours are seen in the carotid
bodies and vagus .

Microscopically, the tumour cells containing neurosecretory

granules are arranged in typical organoid pattern or nests. The
tumour may extend locally to involve the skull and brain but may
rarely metastasise.
 ACOUSTIC NEUROMA (ACOUSTIC SCHWANNOMA).

This is a tumour of Schwann cells of 8th cranial nerve .

It is usually located in the internal auditory canal and

cerebellopontine angle.

It is a benign tumour similar to other schwannomas but by

virtue of its location and large size, may produce compression
of the important neighbouring tissues leading to deafness,
tinnitus, paralysis of 5th and 7th nerves, compression of the
brainstem and hydrocephalus.

REFERENCES:
Pathologic basis of diseases 9th edition by Kumar,Abbas, Fausto.