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anatomy 241 > Lecture 9 - Epithelial tissue and defects in regulation of cell division > Flashcards

Lecture 9 - Epithelial tissue and defects in regulation of cell division Flashcards

1
Q

Role of stem cells

A

Tissue maintenance and renewal

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2
Q

Tissue maintenance and renewal

A

Cells die and are replaced with new cells that are the correct type, in the correct place and in the correct numbers
Stem cells play crucial role in tissue renewal and repair
Disorders of tissue renewal = major medical concern
Misbehaviour of mutant cells underlies the development of cancer

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3
Q

Disorders of tissue renewal =

A

Major medical concern

Misbehaviour of mutant cells underlies the development of cancer

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4
Q

Different tissues at different

A

rates

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5
Q

Tissue renewal and rates

A

Huge variation in rate and pattern of turnover
Cells in epithelial tissues have high regenerative capacity
With adequate nutrition, can replace lost cells by cell division
Causative factors = friction, environmental changes

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6
Q

Stem cells can…

A

repair damaged tissue

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7
Q

All stem cells have three general properties

A

Capable of dividing and renewing themselves for long periods
Unspecialised
Can give rise to specialised cell types

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8
Q

Stem cell types

A

Adult stem cell (somatic cell)

Embryonic stem cells

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9
Q

Adult stem cells

A

Adult stem cell (somatic stem cell)
Undifferentiated cell found amongst differentiated cells in tissue/organ
Can renew itself and can differentiate to major cell types of tissue/organ = multipotent
Multipotent = able to generate many types of cells within a restricted tissue family (adult stem cells)

e.g. adult blood stem cells can differentiate into different types of blood cells

Primary roles of adult stem cells in living tissue is maintenance and repair

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10
Q

Multipotent

A

Can renew itself and can differentiate to major cell types of tissue/organ = multipotent
Multipotent = able to generate many types of cells within a restricted tissue family (adult stem cells)
e.g. adult blood stem cells can differentiate into different types of blood cells

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11
Q

Embryonic stem cells

A

Embryonic stem cells (defined by origin - inner cell mass of a blastocyst)
Only found in early embryo stage
Can become all types of cells in the body = pluripotent
Pluripotent = able to generate all tissue types

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12
Q

Pluripotent

A

Can become all types of cells in the body = pluripotent

Pluripotent = able to generate all tissue types

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13
Q

Induced pluripotent stem cells

A

Researchers have also preprogrammed adult cells to become “induced pluripotent stem cells” - induce the expression of four genes within a cell to create this reversal to a stem cell

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14
Q

Skin stem cells

A

Skin stem cells are found in a bulge under the sebaceous gland. These stem cells can then translocate to the basal layer of the epidermis. Other stem cell populations are found that contribute to hair growth. Once they move to this area, you can’t move them again, as they move they show some kind of differentiation to the cell type they are going to but then these cells will repopulate the epidermis and will be replaced again after 2 months as that is the turnover rate

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15
Q

Epithelial stem cells

A

Epithelial stem cells lining the digestive tract occur in deep crypts and give rise to several cell types (absorptive cells, goblet cells, paneth cells, enteroendocrine cells). Intestine cell turnover is a few days

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16
Q

Cells are capable of adapting to …

A

changes in their environment

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17
Q

Homeostatic mechanisms of cells and their ability to adapt to changes in their environment

A

Physiological conditions - to adapt to normal changes

Pathological conditions - to limit damage in response to disease processes

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18
Q

Change in cellular environment - cell cannot adapt

A

Stimulus severe/lethal
Cell injury or death
Tissue renewal or repair

Stimulus mild sublethal-DNA damage
Change in growth pattern
Dysplasia
Neoplasm

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19
Q

Change in cell environment - cell can adapt

A

Change in growth pattern: reversible
Hyperplasia or hypertrophy
Tissue atrophy or cell atrophy
Metaplasia

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20
Q

Hyperplasia

A

Hyperplasia = increase in size of tissue/organ by increased cell production rate (increase in the size of the whole tissue because the cells replicate faster - more of them)

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21
Q

Hypertrophy

A

Hypertrophy = increase in size of tissue/organ by increase of cell size

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22
Q

Tissue/cell atrophy

A

Tissue/cell atrophy = decrease in size

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23
Q

Metaplasia

A

Metaplasia = reversible transition of one cell type to another (one mature cell type to another cell type)

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24
Q

Dysplasia

A

Dysplasia = Presence of abnormal type of cells (e.g. normal layout is different)

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25
Neoplasia
Neoplasia = new, uncontrolled growth of cells (all of the responses above are due to continued stimuli from the environment whereas when we get some neoplasia itself there is some uncontrolled growth there where even if you take away the stimulus the cell still grows
26
Cell response to environment changes
Dependent on nature of stimulus Tolerable environmental changes = alter patter of growth in 3 ways - cell size, cell division, cell differentiation Often these changes can occur in response to normal physiological/endocrine responses over life - concentration of growth factors/expression of growth factor receptors = altered cell growth (e.g. during pregnancy to allow for adaptions for pregnancy, childbirth and lactation)
27
Hyperplasia and hypertrophy
Increase in cell number/cell size Reversible via tissue atrophy (decrease in cell number/size) and cell atrophy (decrease in cell size) Atrophy due to physiological event is termed involution e.g. thymus gland reduction during adolescence Typically reversible after taking the stimulus away then the tissues revert back to their normal size
28
Hyperplasia and hypertrophy - physiological adaptation
Physiological adaptation = Breast epithelial cells increase in size and number during pregnancy under endocrine stimulation
29
Hyperplasia and hypertrophy - pathological adaptation
Pathological adaptation = endometrial cells increase in number under abnormal endocrine stimulation from oestrogen-secreting ovarian tumour (endometrial hyperplasia)
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Metaplasia features
One mature, fully differentiated cell type adopts totally different fully differentiated cell type Morphology changes in response to cellular environment Adaptive response - cells better equipped to withstand new environment (but ultimately the stimulus that is driving this could be negative in the long term) Common in epithelial tissues Metaplasia: exchange of normal epithelium for another type of epithelium. Reversible when stimulus is taken away
31
Barrett's oesophagus
Metaplasia example Metaplastic transformation of the oesophageal lining Squamous epithelium typical of normal oesophagus - helps with friction coming down Columnar cells with goblet cells - typical of intestinal type epithelium (would usually be exposed to gastric acid) appears in its place - this is in response to gastric acid reflex Columnar cells with goblet cells on left, squamous epithelium typical of normal oesophagus on the right
32
Dysplasia features
Presence of abnormal cells Increased rate of cell division coupled with incomplete maturation of immature cells Dysplasia: disordered growth and maturation of epithelium, still reversible if driving factors eliminated
33
Epidermis of sun exposed skin
Dysplasia example Normal skin = stratified squamous epithelium, keratin layer, normally cells mature over time and lose their shape and become flatten and lose their nuclei until they become a dead keratin layer Dysplastic skin = caused by sun exposure, loss of maturation, nuclei present in keratin layer - so in response to exposure we get an increased rate of cell turnover which means that we have cells moving through the layers of the epidermis faster therefore there is not as much time for differentiation and maturation so what you see here is in the keratin layer there are cell with nuclei present which is abnormal
34
Squamous epitheium at columnar juction of cervix, cervical dysplasia and neoplasia
Dysplasia and neoplasia example Normal epithelial layers I the cervix show differentiation of cells from the basal layer to the vagina, as you go through the layers the nuclei become much smaller in size but do not disappear and the cells become flattened Cervical dysplasia can occur with an increased number of the more basal, nucleated cells reaching the vagina There is a spectrum of progression, with the stratified layer losing its differentiation (becoming neoplastic) In response to the abnormal stimulus (particularly the papillomavirus (HPV)) increase in the number of basal cells being produced meaning that these basal cells are able to maintain their morphology and do not mature so we can find a more basal differentiated normal epithelial cell at the layer next to the vagina
35
Ciliated columnar epithelium - Bronchus with the stimulus of cigarette smoke
Stratified squamous epithelium
36
Transitional epithelium in the bladder with the stimulus of trauma of calculus
Stratiefied squamous epithelium
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Columnar epithelium - gland ducts with the stimulus of trauma of calculus
Stratified squamous epithelium
38
Stratified squamous epithelium - oesophagus with the stimulus of gastric acid
Columnar epithelium
39
Neoplasia features
Uncontrolled growth of cells | First step is cellular transformation
40
Neoplastic state
Poorly regulated cell division in which mass of cells form = neoplasm Cellular proliferation and growth occur in absence of any continuing external stimulus (mass of cells takes on intrinsic growth properties and are able to maintain their turnover without cell stimulus. Contrasts with hyperplasia where abnormal proliferation of cells ceases on removal of stimulus Neoplastic cells exhibit various states of differentiation and commonly fail to achieve highly differentiated states Failure of mechanisms controlling cellular proliferation and maturation Changes in the genetic material are transmitted to each new generation of cells within the neoplasm
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Tissue of origin - surface epithelium (squamous) - Benign
squamous cell papilloma
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Tissue of origin - surface epithelium (squamous) - Malignant
squamous cell carcinoma
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Tissue of origin - surface epithelium (transitional) - Benign
transitional cell papilloma
44
Tissue of origin - surface epithelium (transitional) - malignant
transitional cell carcinoma
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Tissue of origin - solid glandular epithelium (thyroid, kidney, liver) - Benign
Thyroid adenoma Renal adenoma Hepatic adenoma
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Tissue of origin - solid glandular epithelium (thyroid, kidney, liver) - Malignant
Thyroid adenocarcinoma Renal adenocarcinoma Hepatic adenocarcinoma
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Benign
Well defined Progress and slow Similar cell type compared to their tissue of origin usually - tumour cells are similar in structure and shape Often encapsulated and kept in one place
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Malignant
Can lack differentiation - wide variety of different cell shapes and different from the original tissue Erratic growth - sometimes it is slow and sometimes it is fast Locally invasive - invades the tissues surrounding them Metastatic
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Invasive neoplasms are
dangerous, often taken on a number of different attributes that allows them to invade the muscle or basal membrane and actually escape from the cell mass and tissue of origin
50
Cellular events needed for metastasis
Detachment from the main neoplasm Change in the expression of the adhesion molecules within the neoplasm which allows them to break away from one another within the tissue, tumour cells can then secrete adhesion molecules which actually allows them to stick to the basement membrane so they stay in one place and then from there they are able to break out of the tissue Breaking through the basement membrane and connective tissue Need proteins to do this such as proteases and blocking the effect of antiproteases Motility Enter passage for movement e.g. blood stream Enter another tissue type - break through various different cell types that make up/encapsulate the other tissue
51
Degrees of invasiveness
Invasion = malignant tumour grow into, and at the expense of, surrounding tissue Primary tumour = main neoplasm (so where the neoplasm actually originated) Secondary tumour = detached neoplastic mass which is not in contact with primary neoplasm (breakaway of these cells so that we have two separate tumour types) Metastases = secondary tumour which has spread by metastasis
52
Invasion
malignant tumour grow into, and at the expense of, surrounding tissue
53
Primary tumour
main neoplasm (so where the neoplasm actually originated)
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Secondary tumour
detached neoplastic mass which is not in contact with primary neoplasm (breakaway of these cells so that we have two separate tumour types)
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Metastases
secondary tumour which has spread by metastasis
56
How tumours spread - how many routes
Local Trans-coelomic Lymphatic Blood-borne therefore there are 4 routes
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Local tumour spread
extends in the tissue they originated in
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Trans-coelomic spread
Spreading through body cavities = peritoneal and pleural
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Lymphatic spread
Spreading through the lymphatic system
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Blood borne spread
Spreading through the blood
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Why is cancer the worst?
Cancer is a disease in which cells escape from normal growth control mechanisms and proliferate in unregulated manner If malignant cells remained in single mass, most cancers would be readily cured by surgical removal Most malignant tumours spawn cells capable of leaving primary tumour mass and enter bloodstream/lymphatic channels, initiating growth of secondary tumours Spread of tumour within the body (metastasis) is why cancer is so devastating
62
Metastatic cells typically show a variety of adaptions
Often gaining these from gathering somatic mutations within that tumour mass and there is selection going on in the tumour that allows those particular cells to spread … Thought to have special cell-surface properties not shared by most other cells in the tumour Must be less adhesive than other cells to break free of tour mass Must be able to penetrate numerous barriers ECM of surrounding connective tissues, basement membranes that line blood vessels etc Must be able to invade normal tissues if they are to form secondary colonies
63
Three ways to classify epithelium
Three ways we classify epithelium - morphologically (shape, layers), surface specialisations (cilia, microvilli), surface (covering) or glandular (secretory)
64
Where would you find stratified squamous epithelium and why?
Where we need a protective surface i.e. where there is friction or rubbing, where we want cells to be able to breakaway and leave the underlying layers intact For example the oesophagus and epidermis
65
What is an example of metaplasia ?
Reversible transition from one cell type to another e.g. columnar epithelium in oesophagus due to gastric reflux etc.

anatomy 241 (29 decks)

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