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Neoplasia Flashcards

1
Q

What is neoplasia

A

New uncontrolled cell growth–> an abnormal tissue mass
Autonomous
Cells undergo neoplastic changes–> which is a result of genetic changes or mutation

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2
Q

In which cells do neoplasms usually occur

A

From cells that normally have proliferative capacity= Labile cells

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3
Q

What are stabile cells

A

Cells that stop dividing when growth stops
But can regenerate–> hence is injury occurs
E.g. liver cells, kidney, smooth muscle cells, vascular endothelium

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4
Q

What are permanent cells

A

Permanent cells–> don’t change throughout lifetime
Have varying differentation (well and poor differentiated)
Therefore no neoplasms
i.e. mature neurons, cardiac and skeletal myocytes

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5
Q

What are 2 types of neoplasia

A

Benign and Malignant
Both have 2 basic components:
1. Proliferating neoplastic cells–> their parenchyma
2. Supportive stroma–> connective tissue and BV’s

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6
Q

What is benign neoplasia

A

Cells growth that s localised–> encapsulated
Does not penetrate or invade
Does not metastisize (move)- cohesion
Usually well differentiated

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7
Q

What is malignant neoplasia

A 
Cell growth invades adjacent tissue
Erractic growth (asymmetrical)
Slow to rapid mitotic growth
Metastisize (move to different site)--> hence poor cohesion
usually poor differentiation
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8
Q

What is the nomenclature for benign neoplasm

A

Tissue + ‘oma’

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9
Q

What are some harmfull effects of benigns

A

Create pressure on surrounding vital organs
Extra horonal secretion–> endocrine tumours= hyperpituitarism
Secondary complications becomes necrotic:
Can cause haemorrhage
Create ulceration
Create infection/inflammation

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10
Q

What are carcinomas

A

A type of malignant neoplasm
from epithelial cell origin–> any of the 3 germ layers
Tissues and organs develop from epiderm/sctoderm, mesoderm, endoderm

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11
Q

What are sarcomas

A

A type of malignant neoplasm
From mesenchymal cell origin==> the connective tissues, blood vessels, lymph
E.g. fibrosarcoma, liposarcoma

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12
Q

What does differentiation mean

A

degree to which tumour cells ‘cease to’ resemble, comparable to normal cells
both structurally and functionally

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13
Q

What does well differentiated mean

A

cells resembling mature normal cells of tissue of origin of neoplasm= easy diagnosis

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14
Q

What does poorly/undifferentiated mean

A

Primitive unspecialised cells–> hard diagnosis

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15
Q

What does anaplasia mean

A

the degree to which tumour cells function cease to resemble the comparable normal cell function

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16
Q

What does metastases mean

A

development of secondary malignant growths at a distance from primary site
the movement of a malignant neoplasms to a new site
hence tumour implants are discontinuous with primary site
Malignant
Majority cancers metastasize (except BCC)
Breast to bone is a common metastases

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17
Q

What is direct extension in metastases

A

Direct extension

By penetration creating fistulas

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18
Q

What is direct seeding in metastases

A

Across cavities
E.g. Pleural (lung), pericardial, thoracic, abdominal etc
Stomach cancee goes to ovary

19
Q

What is lymphatics metastases

A

most common spread of cancer
follows natural drainage
Skip metastases, venous lymphatic anatomose, inflammation/radaition destroys lymphatics
Nodes enlarged in proximity of cancer

20
Q

What is haematogenous in metastases

A

transfers via blood
Typical of sarcomas
Penetration of veins and arteries (more likely veins coz thinner walls?)
Venous drainage site of neoplasm

21
Q

How do you determine grade of cancer

A

Grade is based on:
Differentiation of tumour cells
Number of mitosis within tumour both presumably correlate with aggressiveness of tumour
Differentiation may differ from one area to another as tumour evolves
Usually cancers become more undifferentiated as they progress

22
Q

How do you determine stage of cancer

A

Based on:
Size of primary lesion
Extent of spread of regional lymph nodes
Presence or absence of blood borne metastases
The higher the stage the worse the prognosis

23
Q

What are the 4 stages of growth and development of tumors

A

Transformation: malignant changes in a target cell
Growth of transformed cells
Local Invasion
Distant metastases

24
Q

What are the 2 ways in which transformation of a cell can occur

A

Proto-oncogenes

Anti-oncogenes or Cancer suppressor genes

25
What is proto-oncogenes
It is a normal gene which when altered by mutation, becomes an oncogene Activated by mutation or increased expression Converted proto-oncogenes become/are oncogenes Oncogenes promote extra or inappropriate cell proliferation Only 15-20% human tumours contain activated oncogenes
26
What is anti-oncogene suppressor/cancer suppressor gene
Some cancers aarise not by activation of growth promoting genes, but by inactivation of genes Normally suppressing cell proliferation Influence only felt when absent Growing evidence that loss of suppressor genes is the underlying mechanism to, malignant transformation
27
What are some factors that can cause the transformation in cells
Chemical carcinogens Radiant Energy Oncogenic viruses
28
Explain the effect of chemical carcinogens
Different chemicals affect different tissues Complete carcinogens= ability to induce tumors without added factors Incomplete carcinogens= only capable of initiation DNA is the primary target for chemical carcinogens Chemical carcinogens induce mutations in proto-oncogenes to become oncogenes to lead to abnormal growth and differentiation
29
Explain the effect of radiation carcinogenesis
Radiant energy--> U.V sunlight, ionizing electromagnetic (both produce neoplasms of all cell types) Has a latency and cumulative effect Possible additive and synergistic effects with other potential carcinogens Action of radiant energy implicates damage to DNA
30
How do U.V. rays affect cells
Squamous Cell Carcinoma (S.C.C)/ Basal Cell Carsinoma (B.C.C)/ Melanocarcinoma of skin (melanoma) Dependent on the dosages/exposure and melanin in skin Effects on cell: Inhibition of cell division Inactivation of enzymes Induction of mutations Enough dosage kills cells
31
Hoe does ionizing radiation affect cells
X-rays and gamma rays Is carcinogenic Chromosomal breakages/translocations/point mutations (DNA injury) Alters proteins Inactivates enzymes Injures membranes Carcinogenicity correlates with its mutagenicity Mutagenicity depends on: Quantity/does of radiation Quality (high v/s low) does rate (divided does allows cellular recovery) DNA repair Host factors (immune status, hormonal influence, cell types, adults/embryonic)
32
What are soe examples of radiation induced cancers
1. Leukaemias 2. Cancer of thyroid 3. Cancer of breast/lung/salivary glands Skin/bone relatively resistant to radiation
33
Explain the effect of oncogenic carcinogens
transformation of cells DNA and RNA oncogenic viruses--> some virues associated with cancer One example of DNA oncogenic virus= HPV Transmission of HPV= SCC of cervix in 90%; associated with sexual activity, also non-sexual transmission
34
Explain the growth of transformed cells
``` Feature of neoplasms: growth is uncontrolled and exceeds growth of normal tissue Cancers are generally- monoclonal= a transformed single cell 1 cell = 30 doublings= 10^9 Growth fraction (GF)= proportion of cells within tumor population that are in the proliferative pool, majority cells in clinically detectable tumour tumour growth= the imbalance between cell production and cell loss ```
35
What is the rate of tumour growth
``` Dependent on the growth fraction (GF) and the degree of imbalance b/c proliferation and loss Some neoplasms (leukaemia/lung Ca) have high growth fraction, t/f rapid clinical course Other neoplasms (breast cancer/colon) have low GF hence slower clinical course ```
36
Explain invasion of cells
In 3 steps: 1. Attachment to basement membranes 2. Secretion of preteolytic enzymes that locally degrade matrix components creating degradation 3. Migration of tumor into degraded ECM zone Cyclic repetition of these 3 steps leas to progressive invasion by advancing tumor cells
37
Explain distant metastases
Malignant cells less cohesive Secretion of factors stimulating own mobility by autocrine mechanisms Vascular dissemination Homotypic adhesions of tumor cells only Hetrotypic adhesions of tumur cells and platelets= enhanced survival and implantation
38
Explain the process of tumour spread
``` Transformation Growth/proliferation and angiogenesis Detachment Invasion Intravasation/release Survival (Host reactions) Arrest Extravasion/invasion Growth/angiogenesis (micrometastasis) Clinically important metastases ```
39
What is radial surgery
the removal of a tuor and a margin of normal tissue around tuour
40
What is a carcinoma in situ
Cancer confined to epithelial surface by basement membrane: Lack of invasion hence metastasis Cytological features of malignancy Considered one step from cancer time leads to penetration of basement membrane
41
What is cancer cachexia
A wasting symdrome--> advanced cancer Survival is weeks/months Range of etabolic, hormonal and cytokine-related abnormalities appear to be a result of interaction b/w metabolically active molecules produced by tumor and the host defense system
42
What are the effects of cancer cachexia
Progressive: Decreased body fat--> increased anorexia Decrease in lean mass Increased weakness (asthenia) Increased constipation Increased anemia Changes in carbohydrate and lipid metabolism Usually ended by secondary infection Some correlation b/w size/extent/severity Pts have higher rates of whole body protein turnover and higer rate of metabolism of all nutrients than non cancer pts Not caused by nutritional commands of tumor Cancers rarely grow as fast as fetus--> yet mothers increases wt
43
What are some reasons for cachexia
Impaired immune system leads to secondary infections Infections lead to debilitation and fever Fever contributes to hypermetabolism Ulcerative lesions from some anemia and weakness Grief and depression from loss of appetite
44
What are common sites of secondary metastases to bone
``` BLT with ketchup and pickle B= Breast L= Lungs T= Thyroid Ketchup= Kidney Pickle= Prostate All the above metastases Spine is the main site for secondary's ```

General Anatomy (13 decks)

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