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57 Cards in this Set
- Front
- Back
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hypertrophy? what muscle? |
an increase in cell size skeletal and cardiac |
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hyperplasia? what organs? |
increase in cell number hormonally sensitive organs: breast, thyroid, endometrium |
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hyperplasia? within what tissues? cause? |
enlargement of gingival tissues epithelium and underlying connective tissue certain drugs |
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atrophy? example of physiological atrophy? causes? |
reduction in cell size by loss of cell substance thyroglossal duct ageing, lack of use/stimulation |
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hypoplasia? what kind of defect? |
reduced size of an organ that never develop to full size developmental defect |
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metaplasia? can be a response to what? example of some areas? can manifest into? and progress to? |
reversible change in which one adult cell type is replaced by another adult cell type adaptive response to stress salivary ducts, barrett's oesophagus, cervix can manifest into dysplasia and progress into malignancy |
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which disorder of growth is not reversible? |
hypoplasia |
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what id dysplasia? what tissues can it be found in? |
pre-malignant process can be found in epithelia - e.g. squamous and glandular |
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atypical alterations in surface epithelium - such as? |
architecture maturation differentiation |
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what is a neoplasm? |
abnormal mass of tissue, growth of which exceeds and is uncoordinated with growth of normal tissue persists in the same manner after stimuli which evoked the change has been removed |
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neoplasia is a result of? |
neoplasia results from the aberration of the normal mechanisms that control cell number, such as cell division and cell apoptosis |
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tumours are monoclonal what does this mean? |
all arise from one parent cell that has undergone a genetic change this change is then passed down to all progeny |
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epidemiology? incidence? prevalence? |
1) study of the distribution of diseases in different populations over time 2) number of new cases 3) number of existing cases |
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what factors to study to understand cancer? |
- geographical distribution - racial prevalence - occupation of those affected |
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risk factors of oral cancer? major & minor |
major: smoking, alcohol, immunosuppression, previous oral cancer minor: oral lesions (leukoplakia), diet, sun exposure |
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benign v.s. malignant: what factors used to differentiate these 2? |
1) growth pattern: well circumscribed? encaupsulated? localized?
2) growth rate 3) clinical effects: hormone secretion? 4) treatment |
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benign v.s. malignant: histogenesis? what factors considered? |
1) histology: resemble tissue of origin? 2) nuclei: regular, small, uniform/pleomorphic? 3) mitoses: normal? or numerous/few? |
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what is prognosis? what information does it give? |
prediction of the probable course and outcome of disease allows the determination of appropriate treatment and estimate survival |
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TNM system? what does it determine and what does it stand for? |
determines tumour stage T = greatest diameter of tumour, structures involved N = lymph node status M = metastasis |
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what are the components of a neoplasm? (5) |
neoplastic cells blood vessels inflammatory cells fibroblasts stroma |
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what are the key elements of cancer development? |
tumour growth: replication, escape from senescence, evasion of apoptosis, limitless replicative potential angiogenesis invasion, metastases +desmoplasia (?) |
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what is desmoplasia |
fibro-connective tissues associated with malignant tumours |
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what are the common sites of metastatic disease |
regional lymph nodes liver lung brain bone skin |
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what are some routes of metastasis? |
- lymphatic (carcinoma) - haematogenous (sarcoma) - across bodily cavities - direct implantation |
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what is the seed and soil hypothesis |
the seed (cancer cell) is dependent on some property of the soil (metastatic site) |
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normall cell ----> transformed cell: what do transformed cells show? |
altered nuclear/cytoplasmic ratio altered DNA content invasive properties, potential to metastasize immortality; do not show senescence |
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aetiology of cancer: what factors involved? |
environmental, genetic, geographical, age, gender |
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aetiology of cancer: what are the environmental factors? |
chemicals: carcinogens from smoking asbestos, nitrosamides radiation: X-ray, UV radiation - skin cancer ionizing radiation viruses: HPV, EBV |
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ionizing radiation: how does it cause cancer? |
ionizing radiation damages DNA, breaks in single/double stranded DNA single: can be repaired but this may be inaccurate, leading to single base mutations double: chromosomal breakage, repair can lead to chromosomal rearrangements |
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viral RNA is copied into DNA by what enzyme before being inserted into host genome? what do viral genes do? |
reverse transcriptase they influence expression of adjacent genes |
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viruses implicated in what human cancers? - HPV - EBV - hep B and hep C |
- cervical cancer - burkitt's lymphoma, hodgkin's lymphoma, nasopharyngeal carcinoma - hepatocellular carcinoma |
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host defences to cancer |
1) cells of immune system - target tumour cells for destruction 2) lymphoid infiltrates common in cancer 3) regression of cancers, such as melanoma |
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what is an oncogene |
an abnormal gene that has the potential to cause cancer |
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what is a protooncogene what happens when it faces a change in DNA sequence? |
normal gene, switched on when cell division is required may give rise to an oncogene, interfering with normal cell regulation |
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what is an oncoprotein |
the abnormal protein expressed by the oncogene |
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what are the 4 types of oncogenes? |
1) genes that produce growth factors 2) genes that produce growth factor receptor 3) genes that encode signal transducers i.e. proteins that transmit the growth signal to the nucleus 4) genes that activate other genes to promote growth (transcription activators) |
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what are some ways oncogenes can be activated? |
1) point mutations 2) gene amplification 3) translocation between chromosomes |
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what is a tumour suppressor gene? |
genes that normally stop a cell from growing, promote differentiation of a cell to a terminal end state trigger checkpoints that cause cell cycle arrest if DNA damage occurs |
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how can tumour suppressor function be lost? needs loss of one/both copies of TSG? |
- inactivating mutations - deletions - viral proteins causing complexes to form (requires loss of bone copies of tumour suppressor gene) |
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examples of tumour suppressor genes |
BRCA-1, BRCA-2 - breast cancer TP53 - Li-fraumeni syndrome Rb - retonoblastoma, osteosarcoma |
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p53: what does it regulate? |
regulates transcription of down-stream target genes (cell cycle arrest, cell death/apoptosis) |
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what are the 3 broad groups of familial cancers? |
1) familial cancer syndromes 2) familial cancers 3) autosomal recessive disorders (due to defects in DNA repair) |
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Li-Fraumeni (TP53) - belongs to which group of familial cancer? |
1) familial cancer syndromes familial retinoblastoma - inheritance of one abnormal copy of Rb |
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breast, colon, ovary cancer - which group of cancer? |
1) familial cancers in some families there is marked increase in incidence of common cancers e.g. BRCA-1 BRCA-2 gene responsible |
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lynch syndrome - which group of cancer? what is it due to? |
lynch syndrome: colorectal cancer, endometrial carcinoma (women) it is a autosomal recessive disorder occurs due to defects in DNA repair |
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what are telomerases? what do they function in? how does this relate to cancer? |
repeating DNA sequences found at the ends of chromosomes important in regulating number of cell divisions a cell is capable of (shortens each time a cell divides until it cannot divide anymore) - tumours appear to express increased telomerase |
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what are epigenetic effects? |
reversible, heritable, altered gene expression without mutation |
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examples of epigenetic events? how are tumour suppressors silenced? |
1)
histone modification DNA methylation 2) silence by hypermethylation |
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molecular carcinogenesis - what does it involve? |
multiple genetic abnormalities involve both oncogenes and tumour suppressors |
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EGFR in head & neck squamous cell carcinoma - stimulated by? - how does it affect prognosis - what monoclonal antibody to use? |
- stimulated by endogenous ligands-> cell cycle progression - high levels of EGFR, poor pronogsis - cetuximab |
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presentation of cancer? |
- variable may be an incidental finding or the effect of a metastatic lesion - depends on the site |
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what are the various ways a tumour can present? |
as a: - consequence of local disease - consequence of distant spread - non-metastatic lesion of malignancy - incidental finding |
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3 symptoms cancer can present through? |
- asymptomatic (incidental finding) - vague symptom: tiredness, weight loss, fever - specific symptom: related to primary or secondary lesion, skin, rash, paraneoplastic syndrome |
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what is a paraneoplastic syndrome? |
symptoms/syndromes in cancer patients that cannot be explained by the effects of local/distant spread of tumours |
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presentation of oral cancer? |
white patch red/speckled patch lump ulcer often not pain often no signs/symptoms |
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diagnosis methods |
through clinical signs/symptoms cytology histopathology molecular techniques (genetics) biomarkers imaging - CT, MRI |
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treatment? |
curative/palliative? surgery radiotherapy chemotherapy none :( |
