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63 Cards in this Set

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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%