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pathology > neoplasia > Flashcards

neoplasia Flashcards

1
Q

what is a neoplasm

A

new growth
abnormal mass of tissue
unco-ordinated growth, exceed that of normal tissues
persists after removal of stimuli that initiated the change

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2
Q

what are the differences in growth pattern in benign vs malignant?

A

benign-
expansion, encapsulated, localised
malignant-
invasion, no capsule, metastasis

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3
Q

what is the difference in growth rate between benign and malignant?

A

benign=slow

malignant= rapid, variable

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4
Q

what are the differences in histology in benign vs malignant?

A

benign- resemble origin, uniform, few mitoses

malignant- not resemble, pleomorphism, many mitoses

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5
Q

what are the clinical effects of a benign tumour?

A

lump/pressure/obstruction
+/- hormone secretion
tx local excision

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6
Q

what are the clinical effects of a malignant tumour?

A

local pressure, infiltration and destruction, distant metastases
+/- hormone secretion
tx local excision + chemo/radiation

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7
Q

what are the names for a squamous epithelial tumour?

A

benign-papilloma

malignant- squamous cell carcinoma

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8
Q

what are the names for a glandular epithelium tumour?

A

benign-adenoma

malignant-adenocarcinoma

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9
Q

what are the suffixes for a CT tumour?

A

benign- oma

malignant- sarcoma

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10
Q

what tumours cant be benign?

A

lymphoid-lymphoma and haemopoietic - leukaemia

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11
Q

what are the names for melanocyte tumours?

A

benign - melanoma

malignant - melanoma

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12
Q

what are the names for germ cell tumours?

A

benign teratoma

malignant teratoma

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13
Q

describe chemical carcinogens

A

smoking polycyclic hydrocarbons including tars, diet drugs, alcohol, asbestos

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14
Q

what are the stages of carcinogenesis?

A

initiation- carcinogen induces genetic change
promotion- another factor stimulates cell for division
progression- additional mutations resulting in malignancy

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15
Q

what is the latency period?

A

time from promotion to clinical tumour

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16
Q

describe physical carcinogenesis

A 
ionising radiation
damages DNA, causing mutation
radium-> bone + marrow tumour
UV light
damages DNA - skin cancer
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17
Q

what is radiation sensitivity?

A

the most sensitive tissues are those where the cells are rapidly removed, eg, embryonic, haematopoietic organs, gonads

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18
Q

what is viral carcinogenesis?

A

DNA viruses
common, viral DNA inserted into host DNA
RNA viruses
reverse transcribes then inserted

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19
Q

give examples of viruses and their tumours

A

Epstein-Barr = Burkitt’s lymphoma, nasopharyngeal cancinoma
hep B/C - hepatocellular carcinoma
HPV- cervical + oropharyngeal carcinoma

20
Q

give some factors of oral cancer (aetiology)

A 
tobacco- smoking/chewing
alcohol
diet/nutrition
oral hygiene
viruses
immunodeficiency
socioeconomic factors
GORD
21
Q

what is a potentially malignant disorder?

A

indicators of the risk of future malignancies occurring in oral mucosa

22
Q

what is leukoplakia?

A

white patch that cannot be rubbed off or attributed to any other cause-potentially malignant lesion - biopsy

23
Q

what is dysplasia?

A 
abnormality confines to epithelium, underlying tissue not affected
potentially malignant
can affect various epithelial tissues
squamous (oral/cervical)
glandular
transitional eg bladder
24
Q

what are proto-oncogenes?

A 
proto-oncogenes are normal genes which regulate cell division, 
growth factors
gf receptors
signal transducers
control of gene expression
25
Q

what are oncogenes?

A

oncogenes are abnormal variants which produce oncoproteins
tight regulation lost
mutation - increases activity of product
excess normal product- duplication of gene
enhanced transcription
-translocation
chromosome rearrangement

26
Q

what are tumour suppressor genes?

A

act to inhibit cell division and suppress growth
anti-oncogenes
require both alleles to mutate for malignancy
rb onle one allele needed

27
Q

what are inherited factors?

A

genetic susceptibility to cancer
inherited cancer syndromes
familial cancer
defective DNA repair

28
Q

what is p53?

A

guardian of the genome
acts just before the restriction pont
stops cycle to allow DNA repair/ apoptosis
often inactivated in cancer (mutation/deletion/viral)

29
Q

what are the hallmarks of cancer?

A 
growth rate/potential
differentiation
invasion/destruction
avoid apoptosis
angiogenesis
evasion of host defences
cell surface changes
30
Q

what are the modes of malignant tumour spread?

A

local spread, lymphatic spread, blood spread, transcoelomic spread, intraepithelial spread

31
Q

what are patterns of metastases?

A

carcomas- lymphatic/blood

sarcomas-blopd

32
Q

what are some predictable metastases?

A

lung->local nodes, liver, bone ,brain

tongue -> neck nodes, lung, spine

33
Q

how do tumour cells interact with cells and molecules in the local environment?

A

alter adhesion membrane
make poor basement membrane
increase protease prod or reduce inhibitors
alter extracellular matrix

34
Q

what is tumour grading?

A 
biological nature of the tumour
assessment of:
invasion into underlying tissue
cellular atypia
eg numberical, low etc, degree of differentiation
35
Q

what are some characteristics of a cells of a malignant tumour?

A

pleomorphism- cell and nucleus
numerous mitoses
abnormal mitoses
variable differentiation

36
Q

what is cancer staging?

A

describes the extent of severity of a persons cancer

done by physical exams, imaging, lab tests, pathology and surgical reports

37
Q

what is the TNM staging ?system

A

T tumour size
N lymph node involvement
M presence of metastases

38
Q

what are the clinical effects of lung cancer?

A

cough, haemoptysis, chest pain, pneumonia

39
Q

what are systemic effects of cancer caused by?

A

often caused by cytokines/hormones released by tumour/ organ dysfunction

40
Q

give examples of systemic effects of cancer

A

fever, anorexia, weight loss, neurological problems, endocrine syndromes, metabolic effects

41
Q

what is tumour immunology?

A

immune surveillance

can suppress of enhance cancinogenesis

42
Q

how does the immune system recognize tumour cells?

A 
tumour associated antigens(TAAS)
products of mutated genes
overexpressed proteings
viral proteins
oncofetal antigens
43
Q

what is elimination?

A

cell mediated immune response
cytotoxic T-lymphocytes
NKCs - 1st line defence
macrophages

44
Q

what is escape? (evade immune response)

A

cells may acquire molecular changes:
alter tumour antigen expression-lack T recognition
activation of immunoregulatory pathways leading to T unresponsiveness
immunosuppressive factors eg cytokines

45
Q

what is immunotherapy?

A 
using px own immunes response to control and destroy malignant cells:
active immunization
reversal of immunosuppression
adopted cell transfer
strengthening natural immune responses

pathology (10 decks)

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