Upper Airways Flashcards

1
Q

Most common disorders of the nose and accessory air sinuses

A
  • Inflammatory disease, mostly in the form of common cold
  • Most are viral but can be complicated by superimposed bacterial infections
  • Less common=few destructive inflammatory nasal diseases and primary tumors of nasal cavity or maxillary sinus
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2
Q

Inflammations of the upper airways

A
  • Infectious rhinitis
  • Allergic rhinitis
  • Nasal polyps
  • Chronic rhinitis
  • Sinusitis
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3
Q

Infectious rhinitis

A
  • common cold
  • viral cause
  • Major viruses: adenovirus, echovirus, rhinovirus
  • catarrhal discharge
  • initial acute stage: nasal mucosa thickened, edematous, and red; narrowed nasal cavities, enlarged turbinates; may extend to produce pharyngotinsillitis
  • secondary bacterial infection enhances inflammatory reaction and produces mucopurulent or suppurative exudate
  • clears up after 7 days
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4
Q

Allergic rhinitis

A
  • Hay fever
  • initiated by hypersensitivity reactions to allergens
  • Most common allergens: plant pollens, fungi, animals, and dust mites
  • IgE mediated with early and late phase response
  • Mucosal edema, redness, mucus secretion with leukocytic infiltration with prominent EIOSINOPHILS!!
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5
Q

Nasal polyps

A
  • focal protrusions of mucosa caused by recurrent attacks of rhinitis
  • edematous mucosa with loose stroma, harboring hyperplastic or cystic mucous glands, infiltrated with inflammatory cells (neutrophils, eiosinophils, plasma cells with occasional cluster of lymphocytes
  • mucosal covering is intact if no bacterial infection but if chronic, becomes ulcerated or infected
  • multiple or large polyps encroaches airway and impairs sinus drainage
  • Most are NOT atopic!
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6
Q

Acute Sinusitis

A
  • Acute or maxillary
  • Acute preceded by rhinitis but maxillary arises by extension of periapical infection through bony floor of sinus
  • caused by inhabitants of oral cavity
  • nonspecific inflammatory reaction
  • impairment of drainage of sinus by inflammatory edema of mucosa and can produce empyema of sinus leading to accumulation of mucous secretions called mucocele
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7
Q

Chronic sinusitis

A
  • Acute sinusitis sometimes causes chronic sinusitis when there is interferance with drainage
  • Mixed microbial flora, mostly of normal inhabitants of oral cavity
  • severe chronic sinusitis caused by fungi (mucormycosis), especially in diabetics!!
  • Uncommonly can be part of Kartagener syndrome which includes bornchiectasis and situs inversus–secondary to defective ciliary action
  • Most not serious but have potential to spread into orbit or surrounding bone causing osteomyelitis or spread into cranial vault causing septic thrombpphlebitis of dural venous sinus
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8
Q

Necrotizing lesions of the nose and upper airways produced by the following

A
  • Acute fungal infections (mucormycosis) especially in diabetics and imunosuppressed
  • Granulomatosis with polyangiitis
  • Extranodal NK/T cell lymphoma, nasal type
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9
Q

Extranodal NK/T cell lymphoma, nasal type

A
  • lymphoma where tumor cells harbor EBV
  • Asian and Latin American males, 50s or 60s
  • Ulceration and bacterial infection complicate process
  • Used to be rapidly fatal due to uncontrolled spread of lymphoma and penetration into cranial vault or secondary bacterial infection and hematologic dissemination of infection
  • Now, localized cases can be controlled with radiotherapy but relapse and rucrrences are common and associated with poor outcomes
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10
Q

Inflammations of the nasopharynx

A
  • Pharyngitis and tonsillitis
  • caused by rhinovirus, echovirus, adenovirus and less commonly RSV and influenza
  • reddening and edema of nasopharyngeal mucosa with reactive enlargement of tonsils and lymph nodes
  • Bacterial infections can superimpose or may be primary invaders
  • inflamed nasopharyngeal mucosa covered by exudative membrane (pseudomembrane)
  • nasopalatine and palatine tonsils enlarged and covered by exudate
  • enlarged redenned tonsils (reactive lymphoid hyperplasia) with pinpoints of edudate coming from tonsillar crypts (follicular tonsillitis)
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11
Q

Most common cause and other causes of bacterial nasopharyngeal inflammation (pharyngitis and tonsillitis)

A
  • Beta-hemolytic strep is most common cause

- Sometimes staph aureus

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12
Q

Follicular tonsillitis

A

enlarged redenned tonsils (reactive lymphoid hyperplasia) with pinpoints of edudate coming from tonsillar crypts (follicular tonsillitis)

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13
Q

Major complications associated with streptococcal “sore throats”

A

-possible development of rheumatic fever and glomerulonephritis

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14
Q

Tumors of the nose, sinuses and nasopharynx

A
  • Nasopharyngeal angiofibroma
  • Sinonasal (Schnederian) Papilloma
  • Olfactory neuroblastoma (Esthesioneuroblastoma)
  • NUT Midline carcinoma
  • Nasopharyngeal carcinoma
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15
Q

Nasopharyngeal angiofibroma

A
  • Benign
  • highly vascular tumor
  • ADOLESCENT MALES that are fair skinned and red-headed
  • Associated with adenomatous polyps
  • arises within fibrovascular stroma of posterolateral wall of roof of nasal cavity
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16
Q

Nasopharyngeal angiofibroma treatment and prognosis

A
  • Surgery
  • But since locally agressive and intracranial extension occurs, recurrence rates as high as 20%
  • In 9% it is fatal with death from hemorrhage and intracranial extension
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17
Q

Sinonasal (Schneiderian) Papilloma

A
  • Benign neoplasm from respiratory or schneiderian mucosa lining nasal cavity and paranasal sinuses
  • Lesions occur in 3 forms: exophytic (most common), endophytic (inverted; most important biologically), and cylindrical
  • HPV 6 and 11 associated with exophytic and endophytic but NOT cylindrical
  • Adult MALES bw ages of 40 and 60
  • Endophytic most aggressive!
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18
Q

Endiphytic sinonasal papillomas

A
  • Benign but locally aggressive neoplasm occurring in both the nose and paranasal sinuses
  • Papillomatous proliferation of squamous epithelial cells invaginates into underlying stroma
  • high rate of recurrence if not adequately excised with potentially serious complication of invasion of orbit or cranial vault
  • Malignant transformation observed in 10%
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19
Q

Olfactory neuroblastoma (Esthesioneuroblastoma)

A
  • Arise from neuroectodermal olfactory cells present within mucosa, particularly in superior aspect of nasal cavity
  • bimodal age distribution with peaks at 15 and 50yrs
  • presents with nasal obstruction and/or epistaxis
  • one of the small, blue, round cell neoplasm that includes lymphoma, SCC, Ewing sarcoma/peripheral neuroectodermal tumor, rhabdomyosarcoma, melanoma, and sinonasal undifferentiated carcinoma
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20
Q

Olfactory neuroblastoma (Esthesioneuroblastoma) morphology

A
  • made of nests and lobules of well-circumscribed cells separated by fibrovascular stroma
  • contain fibrillary matrix that ultrastructurally corresponds to tangles of neuronal cell processes
  • tumor cells contain membrane-bound secretory granules on EM and express neuron specific enolase, synaptophysin, CD 56, and chromogranin by immunohistochemistry
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21
Q

Olfactory neuroblastoma (Esthesioneuroblastoma) prognosis and treatment

A

-Tx: combination of surgery, radiation therapy, and chemotherapy yields 5-year survival rate of 40% to 90%

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22
Q

NUT Midline carcinoma occurs where? Age of onset and clinical progression

A
  • uncommon
  • occurs in nasopharynx, salivary gland or other midline structures
  • occurs at any age
  • mistaken for squamous cell carcinoma morphologically
  • extremely aggressive and resistant to convential tx
  • Most patients survive for less than a year following diagnosis
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23
Q

NUT midline carcinoma genetics and pathogenesis

A
  • associated with translocations that create fusion genes encoding chimeric proteins comprised of most of NUT, a chromatin regulator, and portion of chromatin reader protein, usually BRD4
  • Drugs that displace BRD4-NUT from chromatin induce NUT midline carcinoma cells to terminally differentiate–process seen in acute leukemias but unusual for epithelial cancers
  • Targeted therapy with BRD4-NUT inhibitors being tested
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24
Q

Nasopharyngeal carcinoma

A
  • distinctive geophraphic distribution
  • close anatomic relationship to lymphoid tissue
  • associated with EBV infection
  • 3 patterns: keratninizing squamous cell carcinomas, nonkeratinizing squamous cell carcinomas, undifferentiated/basaloid carcinomas with abundant non-neoplastic lymphocytic infiltrate (lymphoepithelioma)
25
Q

Three factors that influence the origins of nasopharyngeal carcinomas

A
  • Heridity, age and infection with EBV
  • Africa–most frequent childhood cancer
  • Southern china–common in adults but rarely in kids
  • US–rare in both adults and kids
  • associated with diets high in nitrosamines like fermented foods and salted fish as well as smoking and chemical fumes
  • In nonkeratinizing forms, most patients have anti-EBV antibodies against early antigens or viral capsid antigens
26
Q

Primary nasopharyngeal carcinoma

A
  • often clinically silent for long periods and present with nasal obstruction, epistaxis and metastases to cervical lymph nodes in as many as 70%
  • Radiotherapy is standard Tx
  • 5 year survival is 60% overall
  • 5 year survival for nonkeratinizing is 70% to 98&%
  • 5 year survival for keratinizing form is 20%
  • differences in 5 yr survival bc undifferentiated carcinoma is the most radiosensitive while keratinizing squamous cell carcinoma is least radiosensitive
27
Q

Nasopharyngeal carcinoma morphology

A
  • keratinizing and nonkeratinizing squamous cell lesions resemble other usual well-differentiated and poorly differentiated squamous cell carcinomas in other locations
  • Undifferentiated/basaloid variant made of large epithelial cells with oval or round vesicular nuclei, prominent nucleoli and indistinct cell borders, disposed in a syncytium like array
  • Also have admixed abundant, mature, normal appearing lymphocytes (mostly T cells!)
  • EBV genomes detected in serum by PCR or EBV encoded RNAs like EBER-1 or proteins such as LMP-1 identified in malignant epithelial cells by in situ hybridization or immunohistochemistry
28
Q

Most common disorders of the larynx are

A

inflammatory

-tumors are UNCOMMON but are amenable to resection which results in loss of natural voice

29
Q

Causes of laryngitis

A
  • allergic, viral, bacterial or chemical insult but more commonly part of generalized upper respiratory tract infection or result of heavy exposure to environmental toxins like tobacco smoke
  • also occur in association with gastroesophageal reflux due to irritating effects of gastric contents
  • Larynx also affected in systemic infections like TB and diphtheria
  • Most cases are self-limited but may be serious, especially in childhood when mucosal congestion, exudation or edema may cause laryngeal obstruction
30
Q

Laryngoepiglottitis–common in? caused by?

A
  • infants and young children
  • caused by Respiratory syncytial virus, Haemophilus influenzae or B-hemolytic streptococci induces sudden swelling of epiglottis and vocal cords
  • Medical emergency!
  • Uncommon in adults because of larger size of larynx and stronger accessory muscles of respiration
31
Q

Croup

A

-laryngotracheobronchitis in children where the inflammatory narrowing of the airway produces inspiratory stridor

32
Q

Most common form of laryngitis seen in heavy smokers predisposes to

A

-squamous epithelial metaplasia and sometimes overt carcinoma

33
Q

Reactive nodules

A
  • also called polyps
  • develop on vocal cords, mostly in smokers or people who impose great strain on their vocal cords (singer’s nodules)
  • Nodules are bilateral lesions, polyps are unilateral
  • Adults mostly affected
34
Q

Reactive nodules morphology

A
  • smooth , rounded, sessile or pedunculated excrescences, only a few mm in dimension located on true vocal cords
  • covered by squamous epithelium that may become keratotic, hyper plastic, or slightly dysplastic
  • core of nodule is a loose myxoid connective tissue that may be variably fibrotic or punctuated by many vascular channels
  • When nodules on opposing vocal cords impinge on each other, the mucosa may undergo ulceration
  • Bc of their strategic location and inflammation, they change the character of the voice and cause progressive hoarseness
  • NEVER GIVE RISE TO CANCERS!!
35
Q

Laryngeal squamous papillomas

A
  • benign neoplasms on true vocal cords
  • form soft, raspberry like proliferations rarely more than 1 cm in diameter
  • when the papilloma is on free edge of vocal cord, trauma may lead to ulceration that can be accompanied by hemoptysis
36
Q

Laryngeal squamous papillomas histology

A

-made up of multiple slender, finger-like projections supported by central fibrovascular cores and covered by an orderly stratified squamous epithelium

37
Q

Laryngeal squamous papillomas adults vs children? Caused by?

A
  • Papillomas are usually SINGLE in adults but MULTIPLE in children (juvenile laryngeal papillomatosis)
  • BUT multiple recurring papillomas also occur in adults
  • Lesions are caused by HPV 6 and 11
  • Often spontaneously regress at puberty but some affected endure many surgeries before this occurs
38
Q

Carcinoma of the larynx is typically what kind and found in who?

A

-squamous cell carcinoma seen in male chronic smokers

39
Q

Carcinoma of the larynx–Sequence of Hyperplasia-Dysplasia-Carcinoma

A
  • spectrum of epithelial alterations in larynx

- hyperplasia, atypical hyperplasia, dysplasia and carcinoma in situ to invasive carcinoma

40
Q

Carcinoma of the larynx morphology

A

-epithelial changes from smooth, white or reddened focal thickenings, sometimes roughened by keratosis, to irregular verrucous or ulcerated white-pink lesions

41
Q

Gradations of epithelial hyperplasia of true vocal cords

A
  • likelihood of development of overt carcinoma directly proportional to grade of dysplasia when lesion first seen
  • Orderly hyperplasia=no potential for malignancy
  • mild dysplasia=risk rises to 1% to 2% during span of 5-10 years
  • severe dysplasia=risk rises to 5-10%
  • only histologic evaluation can determine gravity of changes
  • changes above are related to tobacco smoke with risk related to level of exposure; changes regress after cessation of smoking up to point of cancer
42
Q

Carcinoma of larynx risk factors

A
  • smoking and alcohol increase risk substantially!!

- Other contributors= nutritional factors, exposure to asbestos, irradiation, infection with HPV

43
Q

laryngeal carcinomas morphology

A
  • 95% are typical squamous cell tumors
  • usually develops on vocal cords but can be above or below cords, on epiglottis or aryepiglottic folds or in pyriform sinuses
  • Those confined within larynx proper are INTRINSIC; those arising or extending outside are EXTRINSIC
44
Q

Squamous cell carcinomas of the larynx growth pattern

A
  • similar to other squamous cell carcinomas
  • Begin as in situ lesion that later appear as pearly gray, wrinkled plaques on mucosal surface, ultimately ulcerating and fun gating
45
Q

Anaplasia of laryngeal tumors

A
  • highly variable
  • sometimes massive tumor giant cells and multiple bizarre mitotic figures seen
  • adjacent mucosa can demonstrate squamous cell hyperplasia with foci of dysplasia or even carcinoma in situ as expected with lesions going from recurrent exposure to carcinogens
46
Q

Carcinoma of larynx clinical course

A
  • seen mostly in men in the sixth decade of life
  • manifests as persistent hoarseness, dysphagia, dysphonia
  • Prognosis is dependent on clinical staging
  • Tx: organ preservation techniques (laser surgery, microsurgery, radiation therapy) being used with greater frequency especially with early disease
  • Combined chemotherapy and radiation therapy, with or without salvage laryngectomy may be required for more advanced or recurrent disease
47
Q

Most common aural disorders in descending order of frequency

A
    1. Acute and chronic otitis (most often involving middle ear and mastoid), sometimes leading to a cholesteatoma
    1. symptomatic otosclerosis
    1. aural polyps
    1. labyrinthititis
    1. carcinomas largely of external ear
    1. paragangliomas, mostly in middle ear
48
Q

Inflammation of the ear

A
  • otitis media, acute or chronic
  • mostly in infants and children
  • typically viral and produce serous exudate but may become suppurative with superimposed bacterial infection
49
Q

Most common bacteria in otitis media are

A
  • strep pneumonia
  • non-typeable H. influenzae
  • Morexella catarrhalis
50
Q

Repeated bouts of acute otitis media with failure of resolution leads to chronic disease. Causative agent of chronic disease are

A
  • Pseudomonas aeruginosa, Staph aureus or a fungus
  • sometimes a mixed flora is the cause
  • chronic infection has the potential to perforate eardrum, encroach on ossicles or labyrinth, spread into mastoid spaces and even penetrate into cranial vault to reduce temporal cerebrates or abcess
51
Q

Otitis media in diabetic caused by P. aeruginosa

A

-especially aggressive and spreads widely causing destructive necrotizing otitis media

52
Q

Cholesteatomas

A
  • associated with chronic otitis media
  • non-neoplastic, cystic lesions 1 to 4 cm in diameter, lined by keratinizing squamous epithelium or metaplastic mucus-secreting epithelium and filled with amorphous debris (derived from desquamated epithelium)
  • Sometimes contain spicules of cholesterol
53
Q

Cholesteatomas pathogenesis

A
  • not clear
  • proposed that chronic inflammation and perforation of eardrum with ingrowth of squamous epithelium or metaplasia of secretory epithelial lining of middle ear are responsible for formation of squamous cell nest that becomes cystic
  • chronic inflammatory reaction surrounds keratinous cyst
  • sometimes cyst ruptures increasing inflammatory reaction and inducing formation of giant cells that enclose partially necrotic squames and other particulate debris
  • these lesions by progressive enlargement erode into ossicles, labyrinth, adjacent bone or surrounding soft tissue and sometimes produce visible neck masses
54
Q

Otosclerosis

A
  • abnormal bone deposition in the middle ear about the rib of oval window into which the footplate of stapes fits
  • Both ears usually affected
  • At first there is fibrous ankylosis of footplate followed by bony overgrowth anchoring it into oval window
  • degree of immobilization governs severity of hearing loss
55
Q

Otosclerosis clinical course

A
  • begins in early decades of life
  • minimal degrees of derangement exceedingly common in US in young to middle aged adults but more severe symptomatic otosclerosis is relatively uncommon
  • most instances is familial following autosomal dominant transmission with variable penetrance
  • Basis for osseous overgrowth is obscure but appears to represent uncoupling of normal bone resorption and bone formation
  • begins with bone resorption, followed by fibrosis and vascularization of temporal bone in immediate vicinity of oval window, in time replaced by dense new bone anchoring footplate of stapes
  • slowly progressive process over span of decades, leading to marked hearing loss eventually
56
Q

Tumors of the ear

A
  • Epithelial and mesenchymal tumors
  • external, middle and internal ear
  • RARE except for basal cell or squamous cell carcinomas of the pinna (external ear)–>occur in elderly men and associated with sun exposure
57
Q

squamous cell carcinomas of the canal

A

occur in middle aged to elderly women and 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

58
Q

Basal cell and squamous cell lesions of the pinna are

A

-locally invasive but rarely spread!!

59
Q

squamous cell carcinomas arising in external canal

A

may invade the cranial cavity or metastasize to regional nodes accounting for a 5 year mortality of about 50%