Flashcards in Head and Neck Robbins Deck (49):
Dental caries: cause, age, how to treat?
Cause: focal demineralization of tooth structure (enamel and dentin) by acidic metabolites of fermenting sugars made by bacteria; think foods with LARGE AMOUNT OF CARBS!!
Age: think especially BEFORE 35
Treat: oral hygiene and have more fluoride in drinking water (fluoride + enamel = fluroapatite, resistant to bacterial acid degradation)
QandA: you get pulpitis only when vascular pulp of tooth is invaded and you get the inflamm reaction; in dental caries, you get substantial cavity formed in the dentin, making a flask-shaped lesion with a narrow orifice
Gingivitis: cause, age, sequelae, treatment
Cause: plaque (sticky, colorless biofilm that collects b/w and on surface of teeth, with bacteria, salivary proteins, and desquamated epi cells) build-up beneath gumline, leading to gingival erythema, edema, bleeding, changes in contour
Age: adolescence most often
Sequelae: calculus (if plaque is not removed), and potential dental caries formation
Treat: reversible; reduce accumulation of plaque and calculus through brushing, flossing, dental visits
Periodontitis: cause, presentation, sequelae
Cause: inflammatory process typically due to anaerobic and microaerophilic gram-neg flora (e.g. Aggregatibacter actinomycetemcomitans, Prevotella intermedia); due to POOR ORAL HYGIENE
Presentation: someone with systemic disease (AIDS, leukemia, Crohn, DS, sarcoid) or defects with neutrophils
Sequelae: destruction of periodontal ligament leading to loosening and loss of teeth; later infective endo, pulmonary and brain abscesses
Aphthous Ulcers (canker sores): cause, age, appearance, histology, results
Cause: Maybe immunologic disorders (Behcet, celiac, IBD) or familial, leading to superficial oral mucosal ulcerations; etiology UNKNOWN
Age: first two decades of life usually
Appearance: shallow, hyperemic ulcerations with thin fibroinopurulent exudate
Histo: at first mononuclear inflamm infiltrate, with maybe secondary bacterial infection and neutrophilic infiltrate
Results: typically 7-10 days, but could persist for weeks in immunocomp patients
QandA: recurrent, solitary or multiple, small ulcers of oral mucosa (never large, but are annoying and tend to occur when STRESSED, and probably have AUTOIMMUNE origin)
What is a key fibrous proliferative lesion? Give presentation, appearance, histo, treatment
Presentation: gingiva of children, young adults, pregnant women
Appearance: ulcerated, elevated, red to purple; can grow quick!!
Histo: vascular proliferation of organizing granulation tissue with varying degrees of acute and chronic inflammation
Treatment: complete surgical excistion (prevent development into peripheral ossifying fibroma!!)
QandA: reactive vascular lesion; some minor trauma to tissues so nonspecific microorganisms can invade
HSV 1 and 2: cause, age, presentation, histology, sequelae
Cause: the viruses themselves
Age: 2-4 years of age, often asymp and not causing significant morbidity
Presentation: Vesicles and ulcerations of oral mucosa that can progress to painful, red-rimmed, shallow ulcerations
Histo: can have intranuclear viral inclusions or even the production of giant cells (multinucleate polykaryons) which can be diagnosed by Tzanck test
Sequelae: could be reactivation with various mechanisms (could have Herpes labialis) and avoid risk with systemic antiviral therapy
QandA: edge of the ulcer are large, MULTINUCLEATED epithelial cells with "ground glass" homogenized nuclei; these guys will heal spontaneously;
cold sores, fever blisters
Oral candidiasis: cause, types, appearance, sequelae,
Cause: Candida albicans is most common fungal infection of oral cavity (think immune status of patient, C albicans strain, composition of individual's normal flora)
Types: pseudomembranous, erythematous, hyperplastic
Appearance: think pseudomembranous with gray-white inflamm membrane with fibrinosuppurative exudate that CAN BE SCRAPED OFF
Sequelae: normally okay except in immunosuppression setting (BM transplant, neutropenia, chemo, AIDS)
QandA: someone with diabetes; oral lesions as white, slightly elevated, soft patches mainly with fungal hyphae (maybe budding cells with pseudohyphae)
Deep fungal infections can be caused by
histoplasmosis, blastomycosis, coccidioidomycosis, cryptococcosis, aspergillosis; think immunocompromised once again!!
Hairy luekoplakia: cause, appearance, difference with thrush, histo
Cause: EBV in immunocomp patients with distinctive oral lesion on LATERAL BORDER of tongue
Appearance: white, confluent patches of fluffy, hyperkeratotic thickenings, almost always on LATERAL BORDER of the tongue
Diff: CANNOT SCRAPE OFF LESION!!
Histo: hyperparakeratosis and acanthosis with 'balloon cells' in upper spinous layer
Leukoplakias: all should be considered what? Presents where? Histo? Causes
Erythroplakia: causes, appearance, age?
Precancerous; seen in ORAL CAVITY and are white patches or plaques with sharply demarcated borders that could even appear as verrucous plaques; could go from hyperkeratosis to acanthotic to dysplastic to CIS; think SMOKERS who are aged 40-70 and are MALE!!
Same causes as above; appears as red, velvety, eroded area in ORAL CAVITY, with severe dysplasia, CIS, or even minimally invasive carcinoma!!
SCC: some causes, where are they, prognosis, molecular aspects, histo, site of mets
Causes: smoked tobacco and alcohol, actinic radiation (sunlight) for lower lip, other carcinogens, betel quid and paan (India, Asia); think HPV, 16 in particular, in the oropharynx
Where are they: head, neck; tonsils, base of tongue, pharynx
Prognosis: catch it earlier to have greater long-term survival; also, HPV-pos SCC has better outlook than HPV-neg SCC
Molecular: mutations and epigenetic changes build up and oncogenes and tumor suppressor gene expression altered (resistance to cell death, increased prolife, induction of angiogenesis, ability to invade and met) --> think HPV E6 and E7 with p53 and Rb again, along with p16!!
Histo: Lesions in oral cavity early on could be raised, firm, pearly plaques or as verrucous areas, then maybe ulcerated with indurated and irregular borders; you could have or maybe not progression to full-thickness dysplasia (CIS) before invasion of underlying CT stroma
Site of mets: cervical lymph nodes locally, then mediastinal lymph nodes, lungs, liver, bones distantly
Dentigerous cyst main facts
Cause: fluid accumulation b/w developing tooth and dental follicle
Histo: think IMPACTED third molar (wisdom) teeth; thin stratified squamous epi
Treat: complete removal of lesion curative
Odontogenic keratocyst: age, histo, treat, sequelae
Age: 10-40, usually males in POSTERIOR MANDIBLE
Histo: thin keratinized strat squamous epi with prominent basal cell layer
Treat: complete removal of lesion
Sequelae: look for nevoid BCC syndrome (Gorlin syndrome) with mutations in tumor suppressor gene PTCH on chromosome 9q22 if there are MULTIPLE OKC's!!!
Robbins QandA: benign, but can recur if inadequately excised!!
Periapical cyst: differences with other odontogenic cysts, where, results, treatment
Diff: inflammatory in origin
Where: apex of teeth, with pulpitis (inflamm of tooth) due to advanced carious lesions or trauma to tooth
Results: necrosis of pulpal tissue, and chronically can have lesion with granulation tissue and possible radicular cyst formation
Treat: complete removal of offending material and restoration of tooth, or extration
Two common odontogenic tumors are:
1. Ameloblastoma (from odontogenic epi with no ectomesenchymal differentation; use wide surgical resection)
2. Odontoma (extensive depositions of enamel and dentin; use LOCAL EXCISION)
QandA: slow-growing, locally invasive tumors that are usually benign; resembles enamel organ and you have cell nests, the center of which has loosely arranged, large polyhedral cells that resemble the stellate reticulum of the developing tooth
Infectious rhinitis: causes, progression
Causes: adenoviruses, echoviruses, rhinoviruses
Progression: initial acute stage with nasal mucosa thickened, edematous, red, nasal cavities narrowed, turbinates enlarged; THEN could have secondary bacterial infection with mucopurulent or suppurative exudate
Allergic rhinitis: causes, histo
Causes: plant pollens, fungi, animal allergens, dust mites (hypersens reaction)
Histo: leukocytic infiltration with eosinophils and the IgE-mediated immune reaction
Nasal polyps: cause, histo, progression
Causes: recurrent attacks of rhinitis leading to focal protrusions of mucosa
Histo: respiratory epi and contain mucous glands within a loose mucoid stroma; have edematous mucosa and variety of inflamm cells like neutrophils, eosinophils, plasma cells and occasional lymphocytes
Progression: could become ulcerated or infected in long run; could get too large and impair sinus drainage!!
QandA: most polyps arise from lateral nasal wall or ethmoid recess; can have nasal obstruction, rhinorrhea, headaches;
Chronic rhinitis: what does it follow? histo?
Causes: Follows repeated attacks of acute rhinitis
Histo: superficial desquamation or ulceration of mucosal epi and see neutrophils, lymphocytes, plasma cells (think potential microbial invasion)
Sinusitis: causes, potential sequelae
Causes: usually acute or chronic rhinitis first, but maybe maxillary sinusitis with extension of periapical infection through bony floor of sinus
Sequelae: impaired drainage of sinus by inflamm edea of mucosa can produce EMPYEMA of sinus; can get mucocele with accumulation of mucous secretions from obstruction of frontal sinus usually; acute can give rise to chronic sinusitis, caused by fungi or maybe Kartagener syndrome (with bronchiectasis and situs inversus);
think especially OSTEOMYELITIS or going into CRANIAL VAULT, with septic thrombophlebitis of dural venous sinus!!!
Some necrotizing lesions of nose and upper airways are:
1. acute fungal infections (diabetes, immunocomp)
2. Wegener's (look for runny nose, fever, malaise, SADDLE NOSE deformity, patchy infiltrates; C-ANCA!!!
3. Extranodal NK/T-cell lymphoma (tumor cells harbor EBV, so think fifth/sixth decad and Asians or Latin Americans; can go to CRANIAL VAULT or have secondary bacterial infection, but control with RADIOTHERAPY amidst potential relapse/recurrence)
Pharyngitis, tonsillitis: causes, additional issues, sequelae
Causes: rhinoviruses, echoviruses, adenoviruses (less respiratory syncytial and influenza viruses)
Additional issues: reactive enlargement of nearby tonsils and lymph nodes, along with beta-hemolytic strep and maybe Staph aureus superimposed (could see pseudomembrane and exudate, along with enlarged, reddened tonsils, AND follicular tonisillitis)
Sequelae: rheumatic fever and glomerulonephritis in case of Group A strep
Nasopharyngeal Angiofibroma: Cause, where, treatment
Cause: benign, highly vascular tumor usually in ADOLESCENT males who are often FAIR-SKINNED and RED HEADED!!
Where: fibrovascular stroma of posterolateral wall of roof of nasal cavity
Treat: Surgical removal
Sinonasal (Schneiderian) Papilloma: cause, age, main form
Cause: benign neoplasm from respiratory or schneiderian mucosa of nasal cavity and paranasal sinuses with HPV DNA 6 and 11 often seen in endophytic type
Age: adult males, 30-60
Main form: benign but locally aggressive neoplasms in nose and paranasal sinuses (invagination of papillomatous prolif of squamous epi into underlying stroma!!)
Olfactory Neuroblastoma (Estehsioneuroblastoma): cause, age, presentation, histo, markers
Cause: neuroectodermal olfactory cells in mucosa, especially superior aspect of nasal cavity
Age: 15, 50
Presentation: nasal obstruction and/or epistaxis
Histo: one of the small blue round cell neoplasms
Markers: neuron-specific enolase, synaptophysin, CD56, chromogranin by IHC
NUT Midline Carcinoma: what is the pathology? Where? Age?
Translocation of NUT, a chromatin regulator, and portion of chromatin reader protein, BRD4
Where: nasopharynx, salivary gland, or other midline structures in thorax or abdomen
Age: think any age really!!
Nasopharyngeal carcinoma: cause, influence, prevalence, histo, other features, treatment
Cause: Heredity, age, infection with EBV
Prev: Think southern China and adults, or African and children (think nitrosamines in diets, smoking; nonkeratinizing form with anti-EBV Ab's)
Histo: Could detect EBV genomes in serum by PCR, or EBV encoded RNAs like EBER-1 or proteins like LMP-1 can be ID's in malignant epi cells by in situ hybridication or IHC
other features: nasal obstruction, epistaxis, METS TO CERVICAL LYMPH NODES
Treat: Radiotherapy (undiff carcinoma most radiosens!!)
QandA: look for anti-EBV IgA in serum; both the differentiated and undiff nonkeratinizing forms are immunoreactive with Ab's to CYTOKERATINS!!
Laryngitis: causes, who can be affected
Causes: Part of generalized upper RTI, tobacco smoke, GERD; maybe TB or diphtheria;
who: infancy/childhood, worry about mucosal congestion, exudation, or edema and laryngeal obstruction; also laryngoepiglottititis due to respiratory syncytial virus, H influenzae, or beta-hemolytic strep; also CROUP, with children and inspiratory stridor usually caused by PARAINFLUENZA VIRUS; HEAVY SMOKERS!!
Reactive Nodules: Cause, histo, sequeale, who?
Cause: can develop on vocal cords
Histo: squamous epi that could be keratotic, hyperplastic, or even slightly dysplastic
Sequelae: maybe hoarseness
Who: think heavy smokers or those who put great strain on vocal cords (SINGER'S NODULES)
Squamous Papilloma and Papillomatosis: cause, histo, who?
Causes: think HPV types 11 and 6 and lead to benign neoplasms on true vocal cords, with soft, raspberry-like proliferations (multiple in kids, single in adults usually)
Histo: finger-like projections with fibrovascular core and stratified squamous epi
Who: adults, kids (latter juvenile laryngeal papillomatosis); usually WON'T become malignant
Robbins QandA: juvenile laryngeal papillomatosis caused by HPV 6 and 11; frequently recur after excision
Carcinoma of Larynx: HIsto, causes, age, clinically, prognosis
Histo: can have smooth, white or reddended focal thickenings and verrucous or ulcerated white-pink lesions; hyperplasia, atypical hyper, dysplasia, carcinoma in situ, invasive carcinoma
Causes: think SMOKERS!! Alcohol
Age: Men in sixth decade of life
Clinically: hoarseness, dysphagia, dysphonia
Prognosis: depends on clinical staging!!
Inflammation of ear: causes, additional issues, chronic problems
Causes: usually viral with serous exudate in infants and children (otitis media!!!)
Additional: superimposed bacterial infection (strep pneumoniae, H influenzae, Moraxella catarrhalis)
Chronic: Pseudomonas aeruginosa, S aureus, fungus: with perforation of eardrum, spreads to mastoid spaces and goes to cranial vault leading to abscess or temporal cerebritis
QandA: obstruction of the eustachian tube could result from sudden changes in atmospheric pressure, like in a plane or diving; think URTI, acute allergic reaction, or viral or bacterial infection at eustachian tube orifice; look for RESIDUAL, sterile fluid!
Cholesteatoma: causes, histo
Causes: chronic otitis media; a non-neoplastic, cystic lesions 1-4 cm in diameter
Histo: keratinizing squamous epi or metaplastic mucus-secreting epi, filled with AMORPHOUS DEBRIS; maybe see chronic inflammatory reaction surrounding keratinous cyst
QandA: the keratin mass that makes up the cholesteatoma becomes infected and shidles the bacteria from antibiotics
Otosclerosis: cause, pathology, sequelae
Cause: abnormal bone deposition in middle ear about rim of oval window into which footplate of stapes fits
Age: early decades of life
Pathology: uncoupling of normal bone resorption and bone formation
Sequelae: marked hearing loss
QandA: autosomal dominant; most common cause of conductive hearing loss in young and middle-aged adults in US
Branchial cyst (cervical lymphoepi cyst): ound where, origin, age, cyst contents, treat
Found: upper lateral aspect of neck along sternocleidomastoid
Origin: second branchial arch
Cyst contents: Clear and watery, or mucinous
Treat: readily excised
Robbins QandA: think LATERAL location, absence of THYROID tissue, and abundant lymphoid tissue
Thyroglossal duct cyst: origin, treatment?
Origin: thyroid anlage should begin at foramen cecum at base of tongue and move to anterior neck; could get cysts
QandA: Heterotopic functioning thyroid tissue or DEVELOPMENTAL CYST can occur anywhere along the descent, usually at the FORAMEN CECUM of the tongue, and look out for dysphonia, sore throat, awareness of mass in throat
Paraganglioma (Carotid Body Tumor): what are they, pathology, where are they, tumor composition and staining, transmission and age
What: neoplasms of neuroendocrine cells associated with symp and parasymp nervous systems
Pathology: loss of function mutations in genes encoding succinate DH subunits or cofactors
Where: Paravertebral paraganglia (symp connections and chromaffin-positive) and aorticopulmonary chain including the CAROTID BODY (parasymp NS innervation and infrequently release catecholamines)
Tumor comp: red-pink to brown; have nests (zellballen) of round to oval chief cells; staining with CHROMOGRANIN, synaptophysin, neuron-specific enolase, CD56, CD57; the spindle-shaped stromal cells called sustentacular cells are positive for S-100
Transmission and age: fifth/sixth decades, can be single, sporadic, or familial (autosomal dom transmission in MEN2)
Sialadenitis: causes, most common forms, ages, histo, treatment, special form of mucocele
Causes: trauma, viral or bacterial infection, autoimmune
Forms: mucoceles are most common of inflamm salivary gland lesion, with most common viral form being mumps especially in parotids
Ages: look for toddlers, young adults, elderly in mucoceles
Histo: pseudocysts and inflamm granulation tissue with mucin, inflamm cells (macrophages)
Treat: complete excision of cyst and minor salivary gland lobe
Special: ranula (duct of SUBLINGUAL gland damaged)
Robbins QandA: mucocele is due to local trauma in either very young or very old, and think foods, chewing gum, objects of any sort placed in mouth; if oral leukoplaka shows up, think pipe smoking and tobacco chewing
Sialolithiasis and nonspecific sialadenitis: causes, how stones form, additional issues, results
Causes: S aurues, S viridans
How: think obstruction of orifices of salivary glands by impacted food debris or by edema about orifice
Additional: maybe secondary bacterial invasion (long-term phenothiazines that suppress salivary secretion)
Results: overt suppurative necrosis and abscess formation!!!
Likelihood of a salivary gland tumor being malignant
is more or less inversely proportional to the size of the gland
Pleomorphic adenoma: causes, molecular, clinical, treat
Causes: think radiation exposure increasing risk, or chromosomal rearrangement with PLAG1 leading to benign tumors that consist of a mixture of ductal (epi) and myoepi cells and show both epi and mesenchymal differentiation; THINK PAROTID MOSTLY!!
Clinical: painless, slow-growing, mobile, discrete masses
QandA: biphasic appearance with admixture of epithelial and stromal elements and can have islands of chondroid and bone; worry about recurrence if tumor implanted during surgery or tumor nodules left behind grow as recurrences in the scar tissue of the previous operation
Warthin Tumor (Papillary Cystadenoma Lymphomatosum): causes, age, where, hito
Causes: think smokers!!
Age: fifth-seventh decades (more males than females)
Where: think PAROTID GLAND!!
HIsto: double layer of lining cells: upper layer with palisading columnar cells with granular, eosinophilic cytoplasm and lower layer with cuboidal to polygonal cells
QandA: benign neoplasm; can be bilateral or multifocal within the same gland
Mucoepidermoid Carcinoma: Where, molecular, histo, prognosis
Where: usually PAROTIDS!!
Molecular: balanced (11;19)(q21;p13) chromosomal translocation creating fusion of MECT1-MAML2 genes
Histo: think cords, sheets, or squamous, mucous, or intermediate cells together; hybrid cells with mucus-filled vacuoles and can be stained with mucin!!
Robbins QandA: think of malignant neoplasms that arise in minor salivary glands; low-grade with better prognosis than high-grade
Ludwig angina is a
rapidly spreading cellulitis, or phlegmon, which originates in the submaxillary or sublingual space but extends locally to involve both; after tooth extraction, you can have extension into the parapharyngeal space and eventually the carotid sheath
Acute necrotizing ulcerative gingivitis represents
an infection by two symbiotic organisms: one is a fusiform bacillus, the other a spirochete (Borrelia vincentii); look for decreased resistance to infection as a result of inadequate nutrition, immunodeficiency, or poor oral hygiene;
look for punched-out erosions of interdental papillae and spread of the ulceration
Mumps is the most common cause of
deafness among postnatal viral infections; found to be unilateral, wheras with rubella will show bilateral infection of labyrinth with permanent loss of cochlear and vestibular function
Peripheral giant-cell granuloma is an
unusual proliferative reaction to local injury that is seen as a mass on the gingiva or the alveolar process (mass covered by mucous membrane, which can be ulcerated);
look for MULTINUCLEATED GIANT cells embedded in a fibrous stroma!!
Adenoid cystic carcinoma is a
slowly growing MALIGNANT neoplasm of the salivary gland that can invade locally and recur after SURGICAL RESECTION!! Look for tumor cells with small, scant cytoplasm, growing in solid sheets or as small groups, strands, or columns;
think CRIBRIFORM (sieve-like) arrangement!!