neoplasia Flashcards

(45 cards)

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
what are oncogenes?
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
what are tumour suppressor genes?
act to inhibit cell division and suppress growth anti-oncogenes require both alleles to mutate for malignancy rb onle one allele needed
27
what are inherited factors?
genetic susceptibility to cancer inherited cancer syndromes familial cancer defective DNA repair
28
what is p53?
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
what are the hallmarks of cancer?
``` growth rate/potential differentiation invasion/destruction avoid apoptosis angiogenesis evasion of host defences cell surface changes ```
30
what are the modes of malignant tumour spread?
local spread, lymphatic spread, blood spread, transcoelomic spread, intraepithelial spread
31
what are patterns of metastases?
carcomas- lymphatic/blood | sarcomas-blopd
32
what are some predictable metastases?
lung->local nodes, liver, bone ,brain | tongue -> neck nodes, lung, spine
33
how do tumour cells interact with cells and molecules in the local environment?
alter adhesion membrane make poor basement membrane increase protease prod or reduce inhibitors alter extracellular matrix
34
what is tumour grading?
``` biological nature of the tumour assessment of: invasion into underlying tissue cellular atypia eg numberical, low etc, degree of differentiation ```
35
what are some characteristics of a cells of a malignant tumour?
pleomorphism- cell and nucleus numerous mitoses abnormal mitoses variable differentiation
36
what is cancer staging?
describes the extent of severity of a persons cancer | done by physical exams, imaging, lab tests, pathology and surgical reports
37
what is the TNM staging ?system
T tumour size N lymph node involvement M presence of metastases
38
what are the clinical effects of lung cancer?
cough, haemoptysis, chest pain, pneumonia
39
what are systemic effects of cancer caused by?
often caused by cytokines/hormones released by tumour/ organ dysfunction
40
give examples of systemic effects of cancer
fever, anorexia, weight loss, neurological problems, endocrine syndromes, metabolic effects
41
what is tumour immunology?
immune surveillance | can suppress of enhance cancinogenesis
42
how does the immune system recognize tumour cells?
``` tumour associated antigens(TAAS) products of mutated genes overexpressed proteings viral proteins oncofetal antigens ```
43
what is elimination?
cell mediated immune response cytotoxic T-lymphocytes NKCs - 1st line defence macrophages
44
what is escape? (evade immune response)
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
what is immunotherapy?
``` using px own immunes response to control and destroy malignant cells: active immunization reversal of immunosuppression adopted cell transfer strengthening natural immune responses ```