Head and Neck Robbins Flashcards
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
Pyogenic granuloma;
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:
- Ameloblastoma (from odontogenic epi with no ectomesenchymal differentation; use wide surgical resection)
- 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)
