Neoplasia 1 Flashcards

(44 cards)

1
Q

Tumour define

A

any clinically detectable lump or swelling

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2
Q

Neoplasm define

A

Abnormal new growth of cells that persists after stimulus is removed

(Type of tumour)

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3
Q

Oncology define

A

Study of tumours and neoplasms

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4
Q

Benign neoplasm define

A

Gross and microscopic appearances are considered to be innocent

Implying that it will Remain localised will not spread to other sites

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5
Q

Cancer define

A

Layman

Malignant neoplasm

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6
Q

Malignant neoplasm define

A

Abnormal growth of cells that persists after stimulus is removed
Invades surrounding tissues and potential to spread distally

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7
Q

Metastasis define

A

malignant neoplasm that has spread from original site to a new non-contiguous site

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8
Q

What is dysplasia?

A

Pre-neoplastic alteration in which
cells show disorganised tissue organisation (confined to epithelia layer)
Reversible

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9
Q

Appearance dysplasia

A

Pleomorphism
Large hyperchromatic nuclei
High nuclei to cytoplasm ratio

(similar to poor differentiation malignant)

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10
Q

2 sites of malignant neoplasm

A
Primary site (original location)
Secondary site (spread to)
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11
Q

Benign vs Malignant

A

Benign: Remain confined and DO NOT metastasise
Malignant: Invade and DO metastasise

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12
Q

3 features of benign tumours

A
Confined local area growth 
Psuedocapsule (pushing outer margin)
Rarely dangerous (depending on location though)
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13
Q

3 features of malignant tumours

A

Irregular outer margin and shape
Ulcerations and central necrosis
Infiltrative (breach basement membrane)

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14
Q

Differentiation benign vs malignant

A

Benign: well differentiated (resemble parent tissue)

Malignant well-poor differentiated (don’t resemble origin tissue)

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15
Q

Cells with no resemblance to any tissue are called…

A

Anaplastic tissue

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16
Q

What happens as differentiation worsens (poor differentiation)?

A
Increase:
size of nucleus
nuclear to cytoplasmic ratio
nuclear staining (hyperchromasia)
Numbers of mitotic figures 

Abnormal mitotic figures (Benz)
Variation in cell and nuclei shape/size (pleomorphism)

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17
Q

How do clinicians define differentiation?

A

Grades
Higher grade = more poorly differentiated
(eg grade 3 cancer = very poorly differentiated)

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18
Q

Grading breast tissue

A

Grade 1: glandular structure preserved mostly, uniform cells
Grade 2: loss of some glands, cells larger and variable in shape
Grade 3: minimal glands, lots of mitosis, variable cell shape

19
Q

Gleasons pattern

A

Prostate grading

1-5 with worsening gland formation

20
Q

Why is grading important?

A

If later grade, lower chance of survival and determines treatment

eg higher grades need more aggressive treatment

21
Q

Steps of cell becoming neoplastic

A

Normal
Dysplasia
Carcinoma in situ (no breach of BM)
Invasive carcinoma

22
Q

Cervical dysplasia grading

A
Normal
CIN 1 (lower grade, lower 3rd affected)
CIN 2 (moderate, lower 2/3rds affected)
CIN 3 (carcinoma in situ, entire thickness affected)
23
Q

Why do we get neoplasia?

A
Lots of new cells dividing every day 
Introduction of mutations - from INITIATORS
Accumulate 
PROMOTORS cause proliferation
= tumour from clonal expansion
24
Q

What sort of damage causes neoplasia?

A

Non-lethal genetic damage

25
Initiators of mutations include...
Chemicals (eg smoking, alcohol, diet, obesity) Infectious agents (HPV) Radiation Inherited mutations
26
Steps of neoplasm
Initiator = mutation Promotor (proliferation of cells with mutation) Progression (accumulate more mutations to enhance survival)
27
What genes are often affected by cancer causing mutations? (4)
Proto-oncogenes Tumour suppressor genes Genes that regulated apoptosis DNA repair genes
28
What are proto-oncogenes?
Drive proliferation
29
Proto-oncogene mutation do?
Excessive increase in normal functions or give a new function (GAIN OF FUNCTION mutation)
30
Proto-oncogene mutation explained
Proto-oncogene (mutates) --> oncogene --> oncoprotein oncoproteins promote growth without signals now
31
Oncogene importance
Dominate over counterparts (only one allele needs to be affected)
32
Example of PO mutation
BRAF (v600e) mutation
33
Tumour suppressor gene function mutation
Usually stop cell proliferation Mutation = loss of function (fail to inhibit growth) (p53)
34
Mutations needed TSG
Both alleles must be damaged to occur (recessive)
35
Apoptosis regulating genes mutation
Abnormalities = less programmed cell death and enhanced survival of cells
36
DNA repair gene mutations
Loss of function Impair ability for cell to recognise and repair non-lethal genetic damage Cells acquire mutations quicker
37
DNA repair gene mutation known as
Mutator phenotype (marked by genetic instability)
38
How are neoplasms named?
Benign end in -oma ``` Malignant end -carcinoma (if epithelial 90%) or sarcoma (if stromal) ```
39
benign epithelial neoplasms
``` Squamous papilloma (skin) Transitional cell papilloma (bladder mucosa) ``` Adenoma (glands) Cystadenoma (ovary gland)
40
How are polyps of epithelial neoplasms named?
Villous (finger like) Sessile (box) Tubular (polyp of colon)
41
Malignant epithelial neoplasms
Squamous cell carcinoma (skin, lung) Transitional cell carcinoma (bladder) Adenocarcinoma (glandular) Basal cell carcinoma
42
Connective tissue benign neoplasms
``` Leiomyoma (smooth muscle) Fibroma Osteoma Chondroma (cartilage) Lipoma Neuroma Neurofibroma (nerve sheath) Glioma (glial cells) ```
43
Connective tissue malignant neoplasms
``` Leiomyosarcoma (smooth muscle) Osteosarcoma Fibrosarcoma Chondrosarcoma Liposarcoma Malignant glioma ```
44
Germ cell neoplasms malignant vs benign
Malignant teratoma and Seminoma (testes, exception to -oma benign rule, ITS MALIGNANT) Benign teratoma in ovaries = dermoid cyst (benign, follows rule)