Patho/Radio Flashcards
reactive lesions (benign fibroepithelial lesions)
etiology
chronic irritation
pyogenic granuloma vs peripheral fibroma vs irritation fibroma
both gingival
pyogenic - more vascular
peripheral fibroma - more fibrous
irritation fibroma - buccal, more fibrous
denture-induced proliferations
epulis fissuratum, gravidarum
leukoplakia (white plaque)
etiology
cannot be ascribed to any identifiable etiology
leukoplakia (white plaque)
histology
sq hyperplasia w hyperkeratosis (white bc of keratin)
parakeratosis - w nuclei
acanthosis
elongation of rete ridges
most important determinant of premalignant potential
dysplastic features (pleiomorphism, nucleoli, inc mitosis, hyperchromasia)
most common presentation of EARLY ORAL CANCERS
erythroplakia (red plaque)
erythroplakia (red plaque)
histology
thin, atropic epithelium, without keratin
LP with engorged capillaries
erythroplakia (red plaque)
grading
2/3 sq epith replaced by atypical cells = SEVERE
1/3 replaced = mild
full thickness = carcinoma in situ (intact BM/no invasion)
major oral cavity cancer
SCCA
non-keratinizing oral cavity cancer etiology
HPV 16, 18
oral cancer histology
keratin pearls, intercellular bridges (well differentiated)
poorly differentiated if hardly any (more aggressive)
oral cancer treatment (3)
surgery
radiotherapy/chemo
targeted molecular therapy/EGFR targeted drugs
oral cancer prognosis (best and worst)
best - lip
worst - floor of the mouth, base of tongue
most common ODONTOGENIC TUMOR
ameloblastoma
ameloblastoma presentation (lesions)
lytic cysts (soap bubble lesions) - multi-locular radioluscencies (with scalloped margins)
*slow-growing, painless, benign but locally invasive and recurrent
ameloblastoma microscopic landmarks/pathologic hallmarks (3)
peripheral palisading cells
reverse nuclear polarization (nuclei at inner edge)
central stellate reticulum
ameloblastoma treatment (2)
hemimandelectomy
total mandiblectomy
fibrous dysplasia affects
pediatric age group, stops growing near skeletal maturation
ossifying fibroma; osteosarcoma
affects?
OF - middle age
osteosarcoma - late teens/ early 20’s
inflammatory nasal polyps etiology
chronic inflammation (systemic allergies, asthma)
inflammatory nasal polyps histology
PCCE
stroma w edematous inflammatory cells (glistening polyp)
inflammatory nasal polyps treatment (2)
polypectomy
treat underlying cause
inflammatory nasal polyps radio
thinned out skull bones (due to pressure, chronic sneezing?)
tonsilitis etiology (2)
viral
bacterial (b-hemolytic strep most common -> rheumatic fever, rh heart disease)
tonsilitis treatment
medical treatment
tonsillectomy if obstructing airflow (kissing tonsils)
necrotizing lesions (“lethal midline granuloma”) (3)
fungal (mucor - invasive, aspergillus - non-invasive)
auto-immune (wegener’s granulomatosis)
t/nk lymphoma
most neoplasms in nasopharynx are
scca
nasopharyngeal angiofibroma (juvenile angiofibroma) histology
branching thin-walled bv in fibrous stroma
*unilateral
nasopharyngeal angiofibroma treatment
surgery (but complications may arise e.g. hemorrhage)
most common benign nasopharyngeal mass
nasopharyngeal (juvenile) angiofibroma
nasopharyngeal angiofibroma imaging (2)
angiography with contrast
ct/mri: like sinusitis/polyp; bony structures intact
tonsillitis vs asymmetrical tonsils
ddx by persistence of asymmetry
sinonasal (schneiderian) papilloma etiology
hpv 6, 11
sinonasal (schneiderian) papilloma histology
inverting type papilloma: sq invaginates into stroma
sinonasal (schneiderian) papilloma treatment
excision (but formidable; high recurrence)