Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
155 Cards in this Set
- Front
- Back
|
What are the 6 hallmarks of cancer?
|
Growth signal autonomy, evasion of growth inhibitory signals, evasion of apoptosis, unlimited replicative potential, angiogenesis, invasion/metastasis
|
|
|
What is cachexia?
|
Extreme weight loss and emaciation similar to anorexia.
|
|
|
What is the most powerful predictor of cancer survival?
|
TNM stage at time of diagnosis
|
|
|
What does TNM stand for?
|
Tumor Nodes Metastases
|
|
|
T classifications
|
T1 means tumor <2cm, T2 means tumor >2cm but <4cm, T3 means tumor >4cm, T4 means tumor is locally invasive
|
|
|
N classifications
|
N1 means single ipsilateral node <3cm, N2 means multiple nodes, N3 means lymph node >6cm
|
|
|
M classifications
|
M0 means no distant metastases, M1 means distant metastases
|
|
|
What are the characteristics of neoplastic nodes?
|
Fixed, matted, and indurated. Usually won't be painful like infected node would be
|
|
|
Most likely areas of node inflammation
|
Anterior triangles and just above or below the sternocleidomastoid
|
|
|
Which oral cancer site can often give rist to bilateral node metastases?
|
The tongue
|
|
|
What are the important characteristics of a suspicious lesion?
|
Color, symmetry, size, surface texture, contour, and growth pattern
|
|
|
What are the areas of highest incidence of oral cancer?
|
Ventral and lateral surfaces of the tongue and the floor of the mouth.
|
|
|
Are palatal swellings serious?
|
Yes, they should always be considered life threatening until proven otherwise
|
|
|
How can CT be used to help diagnose and stage cancer?
|
It is great for hard tissues, but can help determine extent of infiltration into adjacent tissues
|
|
|
How can MRI be used to help diagnose and stage cancer?
|
MRI shows improved definition of soft tissue instead of bone. It can help discriminate tumor from mucous and can detect bone marrow invasion
|
|
|
How can PET be used to help diagnose and stage cancer?
|
Detects early malignancies by mapping location of over active tissues using radiolabeled glucose tracers.
|
|
|
What tumor markers can be found in the serum?
|
Carcinoembryonic antigen (CEA). Mostly found in colorectal, prostate, and breast cancer pts
|
|
|
What is absolutely required before commencing any cancer treatment?
|
Histological confirmation from biopsy
|
|
|
Should general dentists perform biopsies of suspected malignant lesions?
|
NO!!!! Refer to OMFS
|
|
|
What is the best technique for incisional biopsy?
|
Deep narrow incision to include normal tissue under lesion
|
|
|
What is the most common malignancy in the head and neck?
|
Lip SCC, which has an 85% predilection to the lower lip
|
|
|
Distribution of tongue cancers by anatomic location
|
2/3 on anterior tongue, 1/3 on base of tongue. 50-75% have cervical node metastases at time of diagnosis!
|
|
|
What is the most common intra-oral malignancy?
|
Tongue cancer
|
|
|
Which lymph nodes would likely become invaded secondary to tongue cancer?
|
Submandibular and jugulodigastric nodes
|
|
|
Which oral cancer location is most aggressive and deadly?
|
SCC on floor of mouth
|
|
|
Is hard palate or soft palate SCC more common?
|
Soft palate makes up 75% of palatal SCC cases
|
|
|
Where would you most commonly find gingival SCC?
|
70% will arise in mandibular gingiva
|
|
|
Which infectious agent has been found associated with tonsil cancer?
|
HPV
|
|
|
What are the early signs and symptoms of oral cancer?
|
Persistent red and/or white patch, non-healing ulcer, progressive swelling, unusual surface changes, prolonged hoarseness, and sudden tooth mobility
|
|
|
What are the late signs and symptoms of oral cancer?
|
Paresthesia or dysthesia of tongue or lips, persistent pain, indurated area, cervical lymphadenopathy, airway obstruction, dysphagia, chronic earache, and trismus
|
|
|
When would oral cancer diagnostic adjuncts be best used?
|
Following surgical removal of tumor to check for possible recurrence
|
|
|
What is sensitivity?
|
The probability that someone with the disease will get a positive test result
|
|
|
What is specificity?
|
The probability that someone who doesn't have the disease will get a negative test result.
|
|
|
What is the main problem with brush cytology?
|
It only gets the superficial cells, not the deeper epithelial cells.
|
|
|
Which lesions indicate use of brush cytology before biopsy?
|
Red lesions (but only after 2-3 weeks of observation to see if it persists)
|
|
|
How does toluidine blue work?
|
It selectively stains acid tissue, like neoplastic tissue with increased amounts of DNA.
|
|
|
Is TB staining considered sensitive and specific?
|
Yes, 93-97% sensitivity and 73-92% specificity
|
|
|
What does a pt have to rinse with in order for MicroLux DL to work?
|
1% acetic acid, which dehydrates neoplastic cells and changes refractory properties.
|
|
|
How does VelScope identify abnormal tissue?
|
It uses fluorescence and abnormal tissue won't fluoresce like normal tissue so you see a dark spot
|
|
|
What percent of painless red lesions are pre-cancerous
|
90%
|
|
|
T/F There is suficient data to suggest that alternative screening adjuncts are sufficient means of diagnosis
|
False
|
|
|
What is epidemiology?
|
The study of health events or characteristics or health-determinant patterns in society. Investigates factors that determine the presence or absence of disease.
|
|
|
Where does cancer fall on the list of most common cause of death?
|
Second only to heart disease
|
|
|
What are the 2 biggest risk factors for oral cancer?
|
Tobacco and alcohol use, and diet low in fruits and vegetables
|
|
|
What type of neoplasm dominates in the oral cavity?
|
Squamous cell carcinoma (SCC)
|
|
|
What are some oral cancer preventing nutrients?
|
Non-starchy vegetables, fruits, carotenoids, beta-carotene, Vit C
|
|
|
What is the incidence of oral cancer in the USA?
|
37,000 per year
|
|
|
What percentage of oral cancer pts will die of their disease?
|
~57% (amounts to about 8,000 deaths per year)
|
|
|
Where does oral cancer fall on the continuum of most common cancers?
|
6th most common, about 2.4% of all cancers in US
|
|
|
T/F Almost all new case of oral cancer are associated with common risk factors
|
False, 25% of new cases diagnosed have no risk factors at all
|
|
|
What is a carcinogen?
|
Any agent which is directly involved in promotion of cancer or facilitates its propagation
|
|
|
What are the 2 general classifications of carcinogens?
|
Genotoxic (means it screws up DNA in the nucleus and causes mutations), and non-genotoxic
|
|
|
What are the carcinogen groups?
|
Group 1 is definitely, group 2A is probably, group 2B is possibly, group 3 is not classifiable, and group 4 is probably not carcinogenic.
|
|
|
How are strong carcinogens classified?
|
They are able to produce tumors w/low doses. Examples include PAH, nitrosamines, and aromatic amines.
|
|
|
How are weak carcinogens classified?
|
Produce tumors w/high doses. Example is acetaldehyde
|
|
|
Polycyclic aromatic hydrocarbons (PAC)
|
Representative substance is BaP. Derived from coal sources and found in tobacco. Occupation exposure common (steel, petroleum, power plant, etc)
|
|
|
Nitrosamines
|
NNK and NNN are tobacco specific and are derived from nicotene. Strong carcinogens!
|
|
|
What is the organo-specificity of NNK?
|
The lung
|
|
|
Which carcinogen is considered a causative factor of oral cancer in snuff-dippers?
|
Tobacco specific nitrosamines (NNN and NNK)
|
|
|
What is a DNA adduct?
|
An abnormal piece of DNA covalently-bonded to a cancer causing chemical
|
|
|
What are used as bio-markers for assessing exposure to tobacco smoke carcinogens?
|
DNA adducts
|
|
|
What are the six carcinogens that form DNA adducts?
|
BaP, NNK, NDMA, NNN, ethylene oxide, 4-ABP
|
|
|
What is the main active chemical in marijuana?
|
THC
|
|
|
T/F Marijuana smokers do not exhibit similar symptoms to tobacco smokers
|
False, their symptoms are similar but usually more severe
|
|
|
How much more tar and CO are absorbed by marijuana smokers compared to tobacco smokers?
|
3-5 times greater amount in marijuana smokers. Also, 50% higher concentration of benzopyrene and aromatic hydrocarbons
|
|
|
What are the short term effects of marijuana usage?
|
Dry mouth/throat, increases heart rate, anxiety, and loss of motor coordination.
|
|
|
T/F Smoking 1 to 3 joints/day is equal to smoking 5 to 15 cigarettes/day
|
True, lung damage and potential cancer risk much higher in marijuana users
|
|
|
What is the main carcinogenic effect of alcohol?
|
On its own weakly carcinogenic, but combined with tobacco very synergistic and stronly carcinogenic.
|
|
|
Risk of developing cancer in smokers and drinkers
|
3-9 times greater risk in persons that smoke or drink, 100 times greater risk in persons who smoke AND drink
|
|
|
T/F Alcohol abuse is causally related to cancer of the oral cavity, pharynx, larynx, and esophagus
|
True
|
|
|
What are the possible mechanistic pathways through which alcohol may cause cancer?
|
Contact-related effects, solvent effects on tobacco, induction of microsomal enzymes, generation of radicals, nutritional deficiency, and immune suppression.
|
|
|
What is the main carcinogenic agent derived from alcohol?
|
Acetaldehyde, which is the first breakdwon product of ethanol in the liver. It can form DNA adducts.
|
|
|
What type of cancer is associated most with EBV?
|
nasopharyngeal carcinoma
|
|
|
What type of cancer is most associated with HPV?
|
Oropharyngeal carcinomas (mostly HPV type 16)
|
|
|
How does HPV cause cancer?
|
E6 protein targets p53 for ubiquitination and degredation, so you get loss of major suppressor gene
|
|
|
What diseases are associated with EBV?
|
infectious mononucleosis, Burkett lymphoma, and hairy leukoplakia
|
|
|
T/F Wart causing HPV types such as 1, 2, 6, and 11 are associated with increased risk of cancer
|
False
|
|
|
Which types of HPV are associated with development of cancer?
|
Types 16 and 18 are assoicated with cervical, anal/genital, and head/neck cancer
|
|
|
Which virus replicates exclusively in keratinocytes?
|
HPV
|
|
|
How does H. pylori cause stomach cancer?
|
By weakening the protective mucous layer and allowing acid to injure underlying tissue. Free radicals are also released and cause damage
|
|
|
What conditions predispose to esophageal cancer?
|
Barrett's esophagus, which is a transformation of squamous epithelium to specialed columnar. About 5-10% develop cancer of distal esophagus
|
|
|
What common food preservative is associated with cancer risk?
|
Organic and inorganic nitrites commonly added to meat to make it red
|
|
|
How do nitrites contribute to cancer risk?
|
During cooking nitrites in meat can react with degredation products of amino acids and form nitrosamines.
|
|
|
What is the carcinogen commonly found in fried or overheated carbohydrate foods?
|
Acrylamide, a known animal carcinogen
|
|
|
Which variant of alcohol dehydrogenase is associated with 5x greater risk of cancer?
|
ADH3 only, makes the relative risk=40 as opposed to 13 normally
|
|
|
How does alcohol act synergistically with tobacco?
|
It increases fluidity of membranes and allows greater permebility of carcinogens from tobacco into cells
|
|
|
What is the relative risk of alcohol and tobacco when used together?
|
195 as opposed to 13-15 if used alone
|
|
|
What effect does cigarette smoke have on EGFR?
|
It can cause ligand-independent activation as well as over-expression. This happens in 80-100% of oral cancers.
|
|
|
T/F EGF mutations are more common in smokers
|
False, they occur in 51% of non-smokers and only 4% of smokers???
|
|
|
Describe the autocrine signaling from over-activation of EGFR
|
Increased expression of EGF activates TGF-a and MMP expression, which make more EGF and TGF-a.
|
|
|
How do EGFR and TGF-a influence cell cycle?
|
They up-regulated cyclin D1 and cell proceeds through cell cycle. Also up-regulate Bcl-2 which prevents apoptosis.
|
|
|
How does cyclin D1 regulate cell cycle progression?
|
It phosphorylates Rb, allowing progression from G1 to S phase of cell cycle.
|
|
|
What percent of cancers exhibit over-expression of Cyclin D1?
|
25-70% of all oral cancers
|
|
|
What is the carcinogenic mechanism of cigarette smoke?
|
Smoking activates EGFR --> TGF-a and EGF and MMP's upregulated --> Bcl-2 and Cyclin D1 upregulated --> Rb phosphorylated --> G1 to S progression and evasion of apoptosis
|
|
|
Which tobacco smoke carcinogens effect DNA methylation?
|
PAH and NNN/NNK directly effect DNA methylase and DNA methyltransferase activation
|
|
|
Which nucleotide on DNA can be methylated and what is the effect?
|
C nucleotide can be methylated and it causes tightly coiled DNA that will be down-regulated
|
|
|
How is p53 down-regulated?
|
It has CpG rich exons that can be extensively methylated and thus down-regulated.
|
|
|
What is the most common nucleotide transversion due to tobacco carcinogens?
|
G to T transversion, usually at the methylated CpG sites
|
|
|
How much more likely are p53 mutations in smokers?
|
300% more likely to occur
|
|
|
What is the most commonly deleted gene in head and neck SCC?
|
9p21, which is where p16 is found (an inhibitor of cyclin D1)
|
|
|
What effect does folate have on cancer?
|
Increases growth rate of colon cancers
|
|
|
Is most oral mucosa parakeratinized or orthokeratinized?
|
Gingiva and dorsal tongue are parakeratinized and hard palate is orthokeratinized
|
|
|
How do rete pegs differ in keratinized and non-keratinized oral mucosal surfaces?
|
They are deeper in keratinized itssue such as the gingiva, much more shallow in FOM or ventral tongue
|
|
|
What is a macule?
|
Focal color change, neither raised nor depressed
|
|
|
What is the name of a slightly elevated patch?
|
Plaque
|
|
|
What is a papule?
|
Solid, round, raised area, usually <5mm
|
|
|
What is a nodule?
|
Like a papule, except bigger (>5mm usually)
|
|
|
How do vesicles and bulla differ?
|
Vesicles are usually <5mm and bulla are >5mm.
|
|
|
What is acanthosis?
|
An increase in epithelial thickness due to intercellular edema in the spinous layer
|
|
|
What is pseudoepitheliomatous hyperplasia?
|
Benign, reactive overgrowth of squamous epithelium that can mimic SCC
|
|
|
Is leukoplakia a histologic diagnosis?
|
No, its just a clinical term for a white plaque that can't be wiped off and isn't any other disease
|
|
|
T/F True leukoplakias aren't considered to be potentially pre-malignant lesions
|
False, actually 5-25% are diagnosed as dysplastic and 4% are diagnosed as SCC
|
|
|
What is the greatest risk factor for leukoplakia?
|
Smoking , over 80% of leukoplakias occur in smokers
|
|
|
Which microorganism is associated with leukoplakia?
|
Tertiary syphilis caused by Treponema pallidum and HPV types 16 and 18
|
|
|
T/F Leukoplakias due to mechanical or heat trauma are not reversible and are likely pre-malignant
|
False, they usually reverse after habit cessation and have no malignant potential (not even true leukoplakias)
|
|
|
What is the most common oral pre-malignancy?
|
Leukoplakia, usually located on lip, lateral or ventral tongue, soft palate and FOM
|
|
|
What is PVL?
|
Proliferative verrucous leukoplakia. It is a multifocal verruciform leukoplakia commonly on gingiva. Female predilection.
|
|
|
Histology of leukoplakia
|
Common to see hyperkeratosis, hyperplasia and/or acanthosis. May show dysplasia, carcinom in situ, or SCC
|
|
|
Histology of dysplastic epithelium
|
Enlarged nuclei and cells, hyperchromatic nuclei, pleomorphic nuclei and cells, increased mitotic activity with abnormal mitotic figures, and loss of polarity
|
|
|
How long does it generally take for a leukoplakic lesion to transform to SCC?
|
2-4 years after onset of leukoplakia
|
|
|
What is the gender predilection for SCC?
|
Favors males to females 3 to 1
|
|
|
Lymph node metastases from SCC
|
usually ipsilateral cervical nodes affected, will be firm, hard nodes that are non-tender. 21% of pts will have cervical mets at presentation
|
|
|
What is Tx of choice for SCC?
|
Surgical resection possibly with radiation and/or chemotherapy. May involve neck dissection.
|
|
|
What is a fibroma?
|
It is the most common benign soft tissue lesion of the mouth. Reactive hyperplasia to local irritation or trauma. Proliferation of dense fibrous CT
|
|
|
What is a pyogenic granuloma?
|
Reactive hyperplasia to local irritation or trauma. Proliferation of granulation tissue with CT and capillaries. Usually found on gingiva and will likely bleed easily.
|
|
|
What is an epulis granulomatosum?
|
Its a type of pyogenic granuloma that occurs in healing extraction socket in response to foreign body, usually bone spicule
|
|
|
What is the most common salivary gland tumor?
|
Pleomorphic adenoma, a benign mixed tumor of ductal and myoepithelial cells. Slow growing but can get HUGE
|
|
|
Most common site of pleomorphic adenoma
|
Most common in parotid and more common in superficial lobe than deep lobe
|
|
|
What is the primary Tx for pleomorphic adenoma?
|
Excision of tumor and gland usually. Important to get complete excision to avoid recurrence.
|
|
|
What is an ameloblastoma?
|
Its a benign but locally aggressive neoplasm of odontogenic epithelium. Most of them are solid or multicystic.
|
|
|
What is the most common site for ameloblastoma?
|
Posterior mandible in 85% of cases.
|
|
|
Describe the acute viral syndrome associated with HIV
|
1-6 wks after exposure 50-70% of pts will have non-specific symptoms that resemble mononucleosis
|
|
|
What is the most common symptom of HIV infection during the asymptomatic stage?
|
Persistent neck lymphadenopathy
|
|
|
What is AIDS-related complex?
|
It develops before overt AIDS and usually includes candidiasis, herpes zoster, oral hairy leukoplakia, and weight loss.
|
|
|
EC Clearinghouse group 1 diseases
|
Strongly associated with HIV infection. Includes candidiasis, hairy leukoplakia, Kaposi sarcoma, non-Hodgkin lymphoma, periodontal disease.
|
|
|
EC Clearinghouse group 2 diseases
|
Less commonly associated with HIV. Includes TB, viral infections (HSV, HPV, and VZV), necrotizing ulcerative stomatitis, thrombocytopenia purpura.
|
|
|
EC Clearinghouse group 3 diseases
|
Seen in HIV infection sometimes.
|
|
|
T/F Candidiasis is found in over 90% of AIDS pts
|
True
|
|
|
What type of candidiasis is most common?
|
Erythematous variants, occur when CD4 count <400
|
|
|
What type of candidiasis occurs in pts with CD4 count <200?
|
Pseudomembranous variants
|
|
|
Angular chelitis is thought to be caused by co-infection of which two pathogens?
|
Candida and S. aureus
|
|
|
Which stain would you use to identify candida histologically?
|
Periodic acid Schiff (PAS)
|
|
|
T/F Therer is no problem in prescribing anti-fungal meds to an HIV/AIDS pt
|
False, you need to always consult with their primary care physician first
|
|
|
In what cases would you use a systemic antifungal and which one is DOC?
|
If pt not on HAART, has high viral load, or esophageal involvement. DOC is Fluconazole
|
|
|
T/F NUG and NUP respond well to conventional perio therapy
|
False. Clorhexidine and metronidazole must be used in combination with perio therapy
|
|
|
What is the most common latency site for HSV-1?
|
The trigeminal ganglion
|
|
|
What is a common triger for reactivation of HSV primary infection?
|
UV light exposure
|
|
|
HSV in immunocompromised pts
|
Atypical characteristics, lesions present on K and NK mucosa. Co-infection with CMV common as well.
|
|
|
Histological findings in HSV pts
|
Tzanck cells and viral cytopathic effect (multinucleation, chromatin margination, nuclear molding). These also occur in VZV
|
|
|
What is the DOC for co-infection with HSV and CMV in immunocompromised pt?
|
Ganciclovir
|
|
|
Histological characteristics of hairy leukoplakia
|
Baloon cells with perinuclear halo and chromatin beading in upper epithelial layer.
|
|
|
Histology of HPV
|
Presence of koilocytes in upper epithelial layer (vacuolated cells w/shrunken nuclei)
|
|
|
What is Kaposi's sarcoma?
|
It is a malignant neoplasm of vascular endothelial cells. It is the most common malignancy in HIV pts.
|
|
|
Histology of Kaposi's sarcoma
|
Vascular proliferation with lots of small, slit-like blood vessels and spindled endothelial cells
|
|
|
What is the most common method of HIV diagnosis?
|
Enzyme immunoassay followed by Western blot
|
