benign and malignant neoplasia of urt

8/3/2019 Benign and Malignant Neoplasia of URT

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BENIGN AND MALIGNANT

NEOPLASIA OF URTDr. Sunil


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LECTURE OUTCOMES

Describe the pathogenesis, gross and microscopic

appearances of benign and malignant neoplasia

of the upper respiratory tract.

Clinical features, complications of benign andmalignant neoplasia of the upper respiratory

tract


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RESPIRATORY TRACT DIVISION


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Paranasal sinuses are air filled spaces

lined by respiratory mucosa, located

within skull bones.


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NASAL POLYPS


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NASAL POLYPSAbnormal polypoid structures/lesionsArise from the nasal mucosa or

paranasal sinuses

Left anterior nasal

cavity showing anantro-coanal polyp.

Inferior turbinate

is being pushed to

one side!


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HISTOLOGY OF NASAL POLYPS

This is an image of a

nasal polyp showing

the lining respiratory

epithelium. The

boxes show the (1)normal epithelium,

(2) the thin

collagenous portion

of the polyp and the

(3) edematous area

which would take upmost of the polyp.

The presence of

eosinophils in the

polyp is characteristic


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ETIOLOGY AND PATHOGENESIS

Unknown

Chronic inflammation

Autonomic nervous system dysfunction

Genetic predisposition

Allergic versus non-allergic

Most theories consider polyps to be the ultimate

manifestation of chronic inflammation; therefore,conditions leading to chronic inflammation in the

nasal cavity can lead to nasal polyps


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THE FOLLOWING CONDITIONS

ASSOCIATED WITH MULTIPLE BENIGN

POLYPS

Bronchial asthma - In 20-50% of patients with polyps

Cystic Fibrosis (CF) - Polyps in 6-48% of patients with CF

Allergic rhinitis

Chronic rhinosinusitis

Primary ciliary dyskinesia Aspirin intolerance - In 8-26% of patients with polyps

Alcohol intolerance - In 50% of patients with nasal polyps

Churg-Strauss syndrome - Nasal polyps in 50% of patientswith Churg-Strauss syndrome

Young syndrome (i.e., chronic sinusitis, nasal polyposis,azoospermia)

Non-allergic rhinitis with eosinophilia syndrome

(NARES) - Nasal polyps in 20% of patients with NARES


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THEORIES FOR DEVELOPMENT OF NASAL

POLYPS

Bernsteins

theory

inflammatory changes first occur in the lateral nasal wall orsinus mucosa as the result of viral-bacterial host interactionsor secondary to turbulent airflow

Vasomotor

theory

vasomotor imbalance theory postulates that increasedvascular permeability and impaired vascular regulation causedetoxification of mast-cell products (eg. histamine)

Epithelial

rupture theory

The epithelial rupture theory suggests that rupture of theepithelium of the nasal mucosa is caused by increased tissueturgor in illness (eg. allergies, infections). This rupture leadsto prolapse of the lamina propria mucosa, forming polyps.


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CLINICAL PRESENTATION

Asymptomatic

Airway obstruction

Postnasal drip

Dull headaches Snoring

Rhinorrhoea

Hyposmia / Anosmia

Epistaxis (often other lesion) Obstructive sleep apnoea

Craniofacial abnormalities

Optic nerve compression


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rhinosporidiosis

Allergic fungal

sinusitis

Mucormycosis

rhinocerebral(diabetes)


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PAPILLOMA

Papilloma

Occurs in nose,

sinuses, larynx

(occasionally also in

lower airways

Associated with

human papilloma virus

types 6 and 11

Laryngeal lesions

commoner in children can occlude airway

Three types- Septal,

Inverted and

Cylindrical


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Schneiderian or sinonasal

papillomas Benign tumours

Arise from sinonasal

mucosa

Composed of

squamous/columnar

epithelium HPV types 6 and 11

implicated

3 types

- Fungiform

- Cylindrical

- Inverted (endophytic and

biologically important)

If incompletely excised, it

recurs several times and

with such recurrences

chances of local invasion into

the orbit or cranial vault are

reported! Rarely a frankcarcinoma can occur.


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D/Ds of

nasal

polypoid

tumours

Nasopharyngeal

angiofibroma

Olfactory

neuroblastoma

Lymphoma

(Non-Hodgkins)

Nasopharyngeal

carcinoma

Adolescent

males/androgen

dependent

Benign

Bleeds duringsurgery

Angio-centric

NK- T

celltype

Nasal polypoid

masses


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OLFACTORY NEUROBLASTOMA/

ESTHRIONEUROBLASTOMA

Uncommon

Small, blue, round cell tumour

Resembles neuroblasts proliferating into lobularnests

Arises from neuroendocrine cells

Aggressive

Requires surgery, radiotherapy andchemotherapy

5 year survival rates between 50 to

70%


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NPC

Nasopharyngeal carcinoma-

lymphoepithelioma-like

carcinoma, lymphoepithelioma,

Regauds Type

lymphoepithelioma, Schminckestype lymphoepithelioma,

Great

geographical

variation inincidence

Asia (Far East)

Africa

Sporadicallyelsewhere

Associated with

EBV infection


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Nasopharyngeal carcinoma

in a 62-year-old patient.(a) Coronal PET scan

shows intense FDG uptake

(arrow) in proximity to the

brain.

Malignant epithelial tumor

arising in thenasopharyngeal mucosa,

that includes keratinizing

squamous cell carcinoma

and nonkeratinizing

squamous cell carcinoma(differentiated and

undifferentiated) with

abundant non-neoplastic,

lymphocytic infiltrate.


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NASOPHARANGEAL CARCINOMA

Strong epidemiological and biological association

with Epstein-Barr virus (detectable in tumour)

Other factors diet,smoking

Ageincidence curve bimodal: peaks 1525 yearsand 6069 years

Sometimes familial aggregation

Present with neck node enlargement and/or

nasal symptoms Distant metastases to bone, liver and lungs


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PATHOGENESIS

Evidence strongly suggests combined action of:

genetic predisposition

environmental factors

EpsteinBarr virus (EBV):1115

+ within tumor EBV DNA is homogeneousandclonal

+ expression of specific viral messenger RNAs or

gene products consistently detected

+ EBV in tumor tissue (Immunohistochemical

demonstration of EBER in nasopharyngeal undifferentiatedcarcinoma)

Proposed that:

o tumor initiation requires EBV expression


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CT SCAN


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EXAMINATION AND INVESTIGATIONS

Posterior rhinoscopy: The predilection site is the

anterior top of the nasopharynx and the

pharyngeal recess.

Cervical palpation: enlarged lymph nodes Nasopharyngo-scope or nasoendoscopy

Serological examination of EB virus: EB VCA-

IgA, EB NA-IgA(nuclear antigen)

Imaging: CT,MRI Biopsy of the nasopharynx


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Random blind biopsies taken from nasopharyngeal area

should be taken whenever diagnosis is suspected

particulary from fossa of Rossenmuller.


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HISTOPATHOLOGY

Undifferentiated

Differentiated

(squamous cell)

No prognostic

difference

Tumour frequently has a

dense lymphocyticinfiltrate (it is

sometimes known as

lymphoepithelioma)


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Immunohistochemical demonstration of

EBER in nasopharyngeal non-differentiated

carcinoma


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ANGIOCENTRIC NK/T CELL TYPE

LYMPHOMA

Lethal midline granuloma/midline malignant

reticulosis

3% of NHLs in Asia

Destructive midline mass involving Nasopharynx Less commonly, involves Skin or extranodal sites

such as Testis

Contain EBV episomes


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MICROSCOPY

Tumour cell infiltrate typically

surrounds

and invades small vessels,

leading to extensive ischaemic

necrosis.Mixture of small and large

lymphoid cells or

predominantly large lymphoid

cells.

Cytoplasm of tumour cells

contain large azurophilicgranules


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COURSE AND TREATMENT

Indolent course

Most are aggressive

Poorly responsive to therapy


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The larynx is an air

passage, an organ of

phonation and a

sphincteric mechanism

between the

laryngopharynx and

trachea


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VOCAL CORDS POLYPS

Benign non-neoplastic nodules in smokers and

those putting strain on vocal cords singers

nodules


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Symptom:

Hoarseness or

voice change

Finding:

Nodule: bilateral

opposing knotoccurring

at mid-vocal cord Polyp: erythematous,

smooth, mobile vocal cord

lesion larger than

nodules, but similarlocation


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They are nonneoplastic lesions of the vocal cords vocal

cord nodules/Singers nodules and vocal cord polyps


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Vocal cord nodule/polyp,

also known as singersnodules, is a non-neoplastic

lesion secondary to

inflammation or trauma to

the true vocal cord. There

are four histologic subtypes:

edematous-myxoid, fibrous,

vascular, and hyaline.

However, most polyps show

overlap of these features as

seen in the

photomicrograph, which

demonstrate vascular-hyaline

as well as

edematous-myxoid

composition

HISTOLOGY OF VOCAL CORD

POLYPS


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TREATMENT

Strict voice rest

No whispering

(causes as much

strain as yelling)

Surgical

excisionunder suspension

laryngoscope and

biopsy.


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LARYNGEAL/RECURRENT RESPIRATORY

PAPILOMATOSIS (RRP)

Recurrent respiratory papillomatosis (RRP)

is a disease caused by the human

papillomavirus (HPV).

Warty growths in the upper airway may

cause significant airway obstruction or

voice change

RRP has a bimodal age distribution and

manifests most commonly in children

younger than 5 years (juvenile-onset RRP[JORRP]) or in persons in the fourth

decade of life (adult-onset RRP [AORRP]).


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ETIOLOGY

HPV, the virus associated with cutaneous warts,

genital condyloma, and cervical cancer, causes

RRP.

While more than 20 types ofH

PV can causegenital warts, only 2 of these, HPV-6 and HPV-

11, cause the vast majority of cases of RRP.

The disease associated with HPV-11 is more

severe


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CLINICAL PRESENTATION

Hoarseness is the most common presenting

symptom.

Other symptoms include the following:

* Voice change

* Choking episodes

* Foreign body sensation in the throat

* Cough* Dyspnea

* Inspiratory wheeze

* Stridor


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PATHOLOGY

Under low power, the lesion has a papillary

appearance. This results from the exophytic

growth of keratinized squamous epithelium

overlying a fibrovascular core.

Koilocytes, vacuolated cells with clear

cytoplasmic inclusions, are noted and are

indicative of viral infection. Metaplasia and

dysplasia occur in varying degrees


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LARYNX CARCINOMA

Squamous cell carcinomas comprise 95-98% of all

malignant neoplasms of the larynx.

Approximately 90% carcinoma of larynx occur in

men, with peak incidence between the ages of 55to 65.


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ETIOLOGY

Smoking

Alcohol abuse

Air pollution

Viral infection:HPV16,18 (5%)

Precancerous lesion:

leukoplakia

Exposure toasbestos, irradiation

Nutritional factors


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LARYNGEAL CARCINOMA

98%squamous cell carcinoma

Carcinoma in situ Invasive carcinoma

(69%) (90%)

Supraglottic Glottic Infraglottic

(30%) (60%) (6%)

Intrinsic Confined to larynx proper

Extrinsic- arise or extend outside larynx


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Supraglottic

Glottic portion

Infraglottic


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LARYNGEAL CARCINOMA

Effects by local

tissue destruction

(loss of

voice/hoarseness)

Pain, dysphagia,

haemoptysis

Secondary

infection of the

ulcerating lesion

Neck node

metastases


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HISTOPATHOLOGY OF LARYNGEAL

CARCINOMA

Squamous cell carcinoma of the Larynx


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BEHAVIOUR

Spreads to lymphnodes

Very sensitive to

radiotherapy


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TREATMENT

Surgery, radiation or combination

therapy

1/3rd die of the disease

Usual cause of death- Infection of distalrespiratory passages or wide-spread metastases

and cachexia.

benign and malignant neoplasia of urt

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