00- path 3rd set
Terms
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- key characteristics neoplasia
- autonomous cellular division persisting after cessation of initiating stimuli
- 2 components of tumours
- parenchyma (prolif. neoplastic cells) stroma (conn. tiss & vessels)
- benign tumour of epithelial origin
- papilloma (eg squamous or transitional)
- malignant tumour of epithelium
- carcinoma
- benign tumour of glandular origin
- adenoma
- malignant tumour of glandular origin
- adenocarcinoma
- age effected carcinoma versus sarcoma
- carcinoma 55+, sarcoma usually children
- 3 categories of hereditary cancers
- mutant gene inheritance (autosomal dominant - eg:retinoblastoma), familial (uncommon CA type, prevolent in family), autosomal recessive (need both parental alleles)
- purpose of tumour grading/staging
- mgmt. strategy design/measure, outcome comparison
- tumour level of differentiation
- histological - GRADE
- tumour extent of spread
- clinical - STAGE
- CA grading based on
- cellular comparison to normal cells, and counting mitosis
- well differentiated versus poorly differentiated
- Grade I (less agress) - Grade II(v.aggress)
- staging based on
- size of primary tumour, extent of regional lymph involvement, presence of metastasis
- rule of thumb - benign tumours
- usually well differentiated
- well differentiated means
- cells look like normal mature cells of tissue of origin(eg glandular etc.)
- highly UNDIFFERENTIATED tumour cells called
- ANAPLASIA
- variation in size and shape of tumour cells called
- pleomorphism
- tumour cell nuclei with lots of DNA - dark staining
- hyperchromasia
- 6 morphologic chgs in anaplasia
- pleomorphism, hyperchromasia, lg nuclei, incr. mitosis, giant cells, disturbed orientation
- disorderly growth type that doesn’t nec. lead to CA
- dysplasia
- benign tumour characteristics
- usually slow growing, rim of fibrous tiss (capsule), well defined, easy to remove
- type of benign tumour not well defined
- hemangioma (tum. of blood vessels)
- typical of cancer growth
- infiltrates, invades and destroys nearby tissues, not well demarcated
- type of surgery required for CA and why
- radical surgery - remove nearby “healthy†tissue
- most reliable feature of CA
- invasiveness
- tumour implant distant from primary
- metastasis
- diff. btwn. benign and malignant
- benign - no metastasis
- 3 methods of metastasis spread
- direct seeding, hematogenous, lymphatic
- cavities, seeding of CA
- anywhere a malignant neoplasm penetrates an open field - peritoneum, pericardium, joints, subarachnoid
- lymphatic spread - what CA uses most often?
- most common type of spread, sarcomas also use lymph
- spread through blood
- hematogenous - usually sarcomas
- vessel favoured by hema.spread, and effect on organs
- venous (easier to infiltrate), liver, lungs most effected
- tumour (benign or malig) effects depend on what 6?
- location, impingement; functional activity; bleeding; 2ndary infections; ulcerations; initiation of acute symptoms: rupture or infarct
- example of local effect of benign tumour
- adenoma of pituitary destroying pit. function, causing endocrinopathy
- hormonal effect example - benign tumour
- pancreatic islet tumour, overproduction of insulin, causes deadly hypoglycemia
- wasting syndrome associated with cancer
- cachexia - usually a result of cytokines
- inexplicable syndromes assoc. w cancer
- tumour or spread causes substance imbalance and symptoms
- example of substance imbalance assoc. w cancer
- cushings syndrome - lung or pancreatic CA producing ACTH
- histologic features, squam. cell CA
- sheets or solid nests “mosaic†pattern, intercellular bridges, sometimes keratinized
- term: sm. muscle
- leiomyo
- why necrosis in some CA?
- grow too quickly, outgrow blood supply
- metastatic cascade summ
- subclone cell - locomotion through extracell matrix, find and invade vessel, platelet tumour embolus formed, distant site spread, adhere to basement membrane, invade new tissue
- examples of acquired pre-neoplastic disorders
- chronic wound - cell regeneration, so potential for cancer; smokers - chronic bronchial dysplasia; chronic gastritis (pernicious enemia) - all can become malignant
- risk factor for oral CA
- leukoplakia - incr. risk squamous cell CA
- risk for colorectal CA
- villous adenoma
- basis of carcinogenesis
- non-lethal genetic damage (chem, radiation, viral)
- targets of genetic dmg in cells
- genes: promote or inhibit growth, or apop.regulators
- growth promoting gene
- proto-oncogene
- oncogene does what
- promotes autonomous cell growth
- oncogene is what
- a mutant allele of a proto-oncogene
- example tumour supressor gene
- Rb gene - usually prevents cell cycle which otherwise causes retinoblastoma
- Most common genetic disorder in cancer
- TP53 gene - regulates apoptosis, senses DNA damage and initiates repair
- HER2 gene does what
- protooncogene - produces growth factor. commonly damaged in 20 - 30% of breast cancer cases.
- Type I hypersensitivity
- mast cells, basophiles release vasoactive amines, provoke an immediate (anaphylactic) response - eg food allergy, hay fever - IgE antibodies
- Type II hypersensitivity
- mediated by humoral antibodies which predispose cells to phagocytosis, lysis - complement mediated cytotoxicity - (hemolytic disease of newborn, transfusion reactions) - IgG antibodies
- Type III hypersensitivity
- Immune complex mediated (rheumatoid arthritis, serum sickness) --acute inflammatory response initiated, causing cell injury (in Rheum - fc fragment of IgG antibody)
- type IV hypersensitivity
- cell mediated (delayed hypersensitivity reaction) TCells rather than antibodies. eg tuberculosis.
- what might accompany a type II transfusion reaction
- hemolysis
- what is the last stage in wound healing?
- remodelling
- what type of cancer is xeroderma pigmentosum
- a cancer linked to problems with genetic repair mechanisms - autosomal recessive
- in what vessels does the exudate occur
- post-capillary venules
- what percentage of patients have paraneoplastic syndromes associated with cancer
- 10%