topic 4.3 cell and tissue growth disorders Flashcards
effect on cell when there is changes to the environment
leads to reversable changes to the cell. (adapt to altered env to cope and survive) (eg of adaptions-atrophy,hypertrophy,hyperplasia,metaplasia)
the cell will recover/revert ti normal once stimulus stops
cell unable to adapt suscessfully-> degeneration occurs (breakdown)
what is atrophy
- Definition: shrinkage in size of cells by loss of cell substance in response to a
stimulus. When a sufficient number of cells are involved, the entire tissue/organ
diminishes in size
causes of atrophy
DRAIN-L
disue (cells become smaller because no need to mantain their full size for function)
reduced blood supply: (not enough nutrinets)
aging (cells slow down-become smaller)
inadaquate nutrients (cannot mauntain normal size-> become smaller)
loss of innervation (process of supplying nerves to body) (nerve supply loss-> cell cannot reveice stimulus-> shrink
loss of endocrine stimuation (no hormone stimulation-> cannot maintain size)
what is hypertrophy
Definition: increase in size of cells in response to a stimulus, leading to increase in size of organ and
increased functional capacity. (no new cells, just larger cells)
→ not hyperplasia! But may occur with hyperplasia
causes ofhypertrophy
Physiological (normal, good)
* Increased functional demand (eg. skeletal muscles-> in exercise-> cells need to work harder-> increase in size)
* Specific hormonal stimulation (eg. uterus in pregnancy stimulated by hormone progesterone and estrogen)
Pathological (abnormal,disease-related)
* Adaptive hypertrophy (eg. thickening of walls of hollow muscular organs to meet functional
needs– stomach, ventricles (ventricular hypertrophy bc incresed bp -> need to pump blood with more force), urinary bladder)
* Due to obstruction to outflow: stomach (pyloric obstruction), left ventricle (aortic valve disease),
urinary bladder (urethral stricture) (obstruction-> cell need to work harded to push again it)
- Compensatory hypertrophy (eg. when one kidney is removed, the other kidney enlarges in size, removed due to disease hence pathological
) - Hormonal hypertrophy (eg. excessive growth hormone)- (overstimulate cell-> abnormal growth)
what is hyperplasia
increase in the number of cells, usually in labile cell populations,
resulting in increase in size of organ. May occur with hypertrophy in response to
same stimuli
causes of hyperplasia
Physiological
* Hormonal (eg. glandular epithelium of female breast at puberty, pregnancy; bone marrow in
long-standing anemia) (breast development bc of estrogen hormone)
- Compensatory (eg. when a portion of liver is removed/diseased) (transplant)
Pathological
* Excessive hormonal, growth factor stimulation (eg. endometrium, thyroid gland, adrenal gland) (eg extra TSH-> thyroid hyperplasia)
- Important response of connective tissue cells in wound healing (proliferating fibroblasts and
blood vessels aid in repair, stimulated by growth factors produced by WBCs and by cells in the
ECM) (growth factors->fibroblast aka connective tissue,blood vessle hwlp to repair wound-> scarring (impaired function hence pathological)
what is metaplasia
reversible change in which one adult cell type is replaced by
another adult cell type. New cell type is better able to withstand the
adverse/changed environment
cause of metaplasia
Stimuli causes an adaptive response so that new cell type is better adapted to
the stimulus (eg. transitional epithelium lining of urinary bladder is replaced by
tougher, more protective squamous epithelial cells in response to chronic
inflammation caused by bladder stones)
what is the reversible and non reverssable cell adaptation
reversable: atrophy, hypertrophy, hyperplasia, metaplasia
non reversable: neoplasia
what is neoplasia
An abnormal tissue that grows by cellular proliferation more rapidly than normal, and continues to grow after the stimuli that initiated the new growth ceases.
characteristics of neoplasia
1.Does not revert to normal once stimulus is removed.
- Genetic mutation that resulted in the transformation will be passed on to newcells when neoplastic cells divide.
* Cancer is clonal – all cancerous cells in a tumour are derived from a single cell. (new cell will also contain the mutation causid rapid proliferation)
3.Show partial or complete lack of structural organisation. Lack coordination, go
on growing and dividing in an uncontrolled manner.
* Normal cells – communicate with each other, grow in a coordinated manner
and stop dividing when no more cells are required.
* Growth and division of tumour cells may not be effective, some tumour cells
may be defective and die (necrosis)(black) (cannot get enough nutrients)
4.Tumour cells secrete chemical messengers which encourage new blood vessels to grow from venules and
capillaries in adjacent tissues →angiogenesis (to supply blood to tumor cells)
* Blood vessels in tumours may be irregular and easily compressed, occluded by the pressure of rapidly
proliferating tumour cells (vessels get squeezed, may not even be able to transport nutrients to the cells)
malignsnt vs benign tumor
benign: dont spreaf
malignsnt: are invasive and have the potential to metasize: spread of cancer through invasion of blood vessels to other tissue/organs
benign and malignant surface epthelium tumor nomenclature
benign: papilloma
malignant: carcinoma
benign and malignant glandular epthelium tumor nomenclature
benign: adenoma
maligant: adenocarcinoma
benign and malignant fiborous tissue tumor nomenclature
benign: fibroma
malignant: fibrosarcoma
benign and malignant bone tumor nomenclature
benign: osteoma
malignant: osteosarcoma
benign and malignant cartilage tumor nomenclature
benign: chondroma
malignant: chondrosarcoma
how does malignant tumor cause invasion and metastasis
invasion : extension of the tumour growth into adjacent normal tissue in an irregular manner.
* Cells are able to break through basement membrane.
* Malignant cells do not adhere to basement membrane as well as normal cells.
* Display change in their interaction with surrounding stroma → altered synthesis of enzymes that breakdown basement membrane (wallapaper) and stroma.(wall) (because they cannot adhere-> signals them to be invasive and will start producing enzymes to break down barriers)
* Produce factors that help cells spread. (eg blood vessels)
Metastasis: spread of malignant tumour (primary tumour) from its site of origin to form a secondary tumour.
1. Malignant cells detach from site of origin and migrate through lymphatics, blood vessels and cavities (evade immune system!)
2. As they travel, they may lodge in a vessel wall/cavity wall and pass through the wall. They then migrate through another connective tissue/tissue type to establish at a new site, distant from site of
origin.
** Not all malignant tumours metastasise, and not all circulating cancer
cells are able to successfully pass through vessel walls and grow at a distant site.
what are the routes of metastasis
1.Haematogenous spread (via blood circulatory system): mainly responsible for secondary tumours that grow in liver, lungs, spleen
2.Lymphatic spread (via lymph circulation):
* Lymph vessel walls are thin, lymph flow is low pressure → facilitates spread of tumour cells
* Tumour cells enter lymphatic vessels near site of origin → travel to lymph nodes → establish
secondary tumours within lymph nodes (lymph nodes will appear enlarged).
3.Serosal spread (via serosal surfaces) (Serosae – thin membranes that line body cavities)
* Tumours that form on/near serosal surfaces spread along membranes like scattered seeds.
* Stimulates production of protein-rich exudate.
4.Intra-organ spread (rarely seen)
* Eg. along inner lining surface of trachea
describe immune serveilace against tumor
- Immune surveillance:The host immune system identifies cancerous and/or precancerous cells and eliminates them before they can cause harm.
- Despite tumour immune surveillance, tumours do develop in the presence of a functioning immune system.
- Tumour cells develop different strategies to escape immune surveillance and avoid attack from immune system
what are the phases of immunoediting
- dessignated elimination
- equilibrium
- escape
describe the elimination phase
The elimination phase of cancer immunoediting is exactly the same process described in the initial theory of tumour immune surveillance:
* immune system detects and eliminates tumour cells that have developed as a result of failed intrinsic (built in) tumour suppressor mechanisms.
- The elimination phase can be:
1. complete:when all tumour cells are cleared or
2. incomplete, when only a portion of tumour cells are eliminated. - In the case of partial tumour elimination, the theory of immunoediting is that a temporary state of equilibrium can then develop between the immune system and
the developing tumour. (there is still cancer but its being managed/controlled by immune system)
describe the quilibrium phase in immunoediting
In equilibrium period it is envisaged that tumour cells either remain dormant or continue to evolve, accumulating further changes (such as DNA mutations or changes in gene expression)
* It (tumor cells) leads to modulate (change) the tumour-specific antigens and stress-induced antigens that they express.(cos tumor cells are stress cos thers so many of them, eg cannot get enough o2, they hide thir surafce antigens-> immune cells difficult to identify and detetc them)
* As this process continues, the immune system exerts a selective pressure by eliminating susceptible tumour clones where possible.
* The pressure exerted by the immune system during this phase is sufficient to control tumour progression,
describe the escape phase in immunoediting
But eventually, if the immune response still fails to completely eliminate the
tumour,
* the process results in the selection of tumour cell variants that are able to resist,
avoid, or suppress the antitumor immune response, leading to the escape phase.
* In escape phase the immune system is no longer able to contain tumour growth, and a progressively growing tumour results
If tumour cells express unusual antigens, why are they not regarded
as foreign and attacked by the immune system?
The main problem appears to be that the abnormal molecules are
not appropriately presented to the cells of the immune system, especially
cytotoxic T cells.
* Nevertheless, on occasion, tumour cells may be attacked by NK cells,
cytotoxic T cells, activated macrophages.
* It is likely that the most important of these attackers are NK cells.
what cell is the most imprtant attacker of tumor cells
NK cells
what is NK cell responsible for/what do they do
NK cells effectively kill two types of cellular targets: cells that fail to express MHC class I molecules (if they see that there is MHC class 1, they wont attack) and cells that express certain stress-related proteins.
* Both conditions commonly apply to cancer cells.
* As a result, Nk cells play a key role in the destruction of tumours.
What is the primary goal of surgery in cancer treatment?
To remove cancerous (and sometimes benign) tumours completely.
Can surgery be combined with other cancer treatments?
Yes, surgery is often used alongside radiation therapy or chemotherapy.
How does radiation therapy work?
it works by disrupting DNA inside cell, preventing cell from deviding
what is the purpose of using radiation
to shrink tumor prior to surgery, also can be used post surgery as well
what cells are susceptable to radiation
cells that are rapidly deviding (such as cancer cell), but any cell can be damanged (some permanently)
what is the purpose of using radiation with chemotherapy
some agents, (radiosensitizers) make cells mroe susceptaable to the effects of susequent radiation therapy
how is radiation therpay usually administered
through an external source, like x ray machien. sometimes radioactive material is also implanted into a tumor
what is the main mechanism of chemotherapy
some chemotherpay agents disrupt different phases of the cell cycle while others disrupt specific processes required for cell division.
what are the two examples of chemotherpay drugs
vincristine and doxyrubicin
what is the effect of viscristine
disrupts tubulin which is a part of a cell’s “skeleton” and a component of cell division
what is the effectof doxorubicin
often used with viscristine, doxorubicin is a drug that inhibits enzymes required for DNA duplication which is required for a cell to devide. combinign these drugs attacks a cencaer cells in two dfferent ways
what type of cell is affected by chemotherapy agents
rapidly deviding cells, like cancer cells. rapidly deviding normal cekks are also likely to be affected by cheotherapy agents. eg include cells in bone marrow an intestinal tract, which partially explains common side effects of treatment such as diarrhea and low white blood cell count.
what are other treatment approaches
1.immunotherapy: harnessing the power of an individuals immune system to attack cancer
Cancer cells have developed a variety of strategies to make themselves invisible to the immune system. The goal of immunotherapy is to overcome these defences
- personalised chemotherpy: Customizing treatments based on an individual’s or a tumour’s genetic makeup, tumour type and lifestyle considerations is entering
the mainstream in human medicine. It’s often referred to as personalized or precision medicine
