Cellular Adaptations Flashcards

1
Q

How is cell proliferation controlled

A

Chemical signals which either stimulate or inhibit cell proliferation
When a signalling molecule binds to a receptor, it results in the modulation of gene expression
Receptors usually in cell membrane but can be in the cytoplasm or nucleus

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2
Q

What can chemical signals make the cells do

A

Survive - resist apoptosis
Divide - enter cell cycle
Differentiate - take on specialised form and function
Die - undergo apoptosis

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3
Q

How can a cell population increase its number

A

Shortening the cell cycle or conversion of quiescent (dormant) cells to proliferating cells by making them enter the cell cycle

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4
Q

What do cell checkpoints do

A

Check damage to DNA, all of DNA has replicated
Cell will try to fix it or go into apoptosis
Damaged cells cannot replicate

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5
Q

What is the restriction point

A

Near the end of G1
Majority of cells that pass R point will likely complete cell cycle
Most commonly altered checkpoint in cancer cells
Checkpoint activation delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53
Proto-oncogenes regulate normal cell proliferation

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6
Q

Other than the restriction point, what other cell checkpoints are there

A

G1/S transition -checks for DNA damage before
DNA replication
G2/M transition - checks for DNA damage after
DNA replication

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7
Q

How is the cell cycle controlled

A

Controlled by cyclins binding to cyclin dependent kinases (CDK)
Once CDK is activated, it drives the cell cycle by phosphorylating proteins such as retinoblastoma susceptibility (RB) protein
Cyclin - CDK complex tightly regulated by CDK inhibitors
Growth factors work by stimulating production of cyclin D or inhibiting CDK inhibitors
Once pRb retinoblastoma is inactivated, cell cycle progression occurs
Retinoblastoma normally inhibits restriction point
Tumour suppressor gene

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8
Q

How many times can a cell divide

A

Hayflick limit - depends on telomere shortening

61.3 divisions in humans

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9
Q

How can cells adapt

A

Multiply to replace loses (regeneration)
Increase in number above normal (hyperplasia)
Increase in size (hypertrophy)
Become smaller (atrophy)
Be replaced by a different type of cell (metaplasia)

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10
Q

What is regeneration and give an example

A

Replacement of cell losses by identical cells in order to maintain the size of a tissue or organ
Eg. Replacement or red and white cells in the bone marrow

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11
Q

What types of tissue can regeneration occur in

A

Only occurs in labile and stable cells and where collagen framework is not damaged

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12
Q

What is hyperplasia

A

Increase in tissue or organ size due to increased cell numbers

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13
Q

In which types of tissue can hyperplasia occur in

A

Labile or stabile - only cells able to divide
Caused by increased functional demand or hormonal stimulation
Remains under physiological control and is reversible (unlike neoplasia)
Can occur secondary to a pathological cause but the proliferation itself is a normal response (unlike neoplasia where proliferation is abnormal)
Repeated cell divisions exposes the cell of the risk of mutations and neoplasia

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14
Q

What are examples of physiological hyperplasia

A

Proliferative endometrium under influence of oestrogen

Bone marrow produces erythrocytes in response to hypoxia

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15
Q

What are examples of pathological hyperplasia

A

Epidermal thickening in chronic eczema or psoriasis

Thyroid goitre in iodine deficiency

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16
Q

What is hypertrophy

A

Increase in tissue or organ size due to increased cell size

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17
Q

In which types of tissue can hypertrophy occur in

A

Labile, stable but especially permanent tissues
In labile and stable tissues, hypertrophy usually occurs along with hyperplasia
Like hyperplasia, caused by increased functional demand or hormonal stimulation
Cells contain more structural components - workload is shared by a greater mass of cellular components

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18
Q

What are examples of physiological hypertrophy

A

Skeletal muscle hypertrophy of a bodybuilder and the smooth muscle hypertrophy of a pregnant uterus (which also involves hyperplasia)

19
Q

What are examples of pathological hypertrophy

A
Heart hypertrophy (ventricular hypertrophy) - problem with systemic or valvular heart disease is that it does not rest 
Bladder hypertrophy - with a prostate enlargement, bladder always pushes against it causing hypertrophy
20
Q

What is compensatory hypertrophy

A

Damage to one of 2 organs causes other organ to work harder

eg. removal of kidney

21
Q

Why do athletes not get heart hypertrophy

A

Rest after exercise - are not constantly overstrained

22
Q

What is atrophy

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

23
Q

What is happening in the cell during atrophy

A

Shrinkage in size to the smallest at which it can survive
Reduced structural components of the cell
May eventually result in cell death

24
Q

How does organ/tissue atrophy occur

A

Organ atrophy typically due to combination of cellular atrophy and apoptosis
Reversible up until a certain point

25
Q

What happens in tissue atrophy

A

Reduced supply of growth factors and/or nutrients

Puts parts of cell into autophagosomes called residue bodies

26
Q

What are examples of physiological atrophy

A

Ovarian atrophy in post menopausal women, decrease in size of uterus after childbirth

27
Q

What are examples of pathological atrophy

A

Disuse atrophy - reduced functional demand/workload
Muscle atrophy after disuse - reversible with activity
Denervation atrophy - loss of innervation
Wasted hand muscles after median nerve damage
Inadequate blood supply - thinning of skin on legs with peripheral vascular disease
Malnutrition - wasting of muscles with malnutrition
Loss of endocrine stimuli - breast, reproductive organs
Persistent injury - persistent inflammation, polymyositis (inflammation of muscle)
Ageing = senile atrophy - brain, heart
Pressure - tissues around an enlarging benign tumour

28
Q

What is atrophy of extracellular matrix

A

Lose bone matrix leading to osteoporosis

29
Q

What is metaplasia

A

Reversible change of one differentiated cell type to another

30
Q

How does metaplasia happen

A

Due to altered stem cell differentiation - produce different cells
May represent adaptive substitution of cells that are sensitive to stress by cell types better able to withstand adverse environment
Metaplastic cells are fully differentiated and the process is reversible
Sometimes a prelude to dysplasia and cancer
No metaplasia across germ layers - only from same type of cells
Occurs only in labile or stable cell types
Involves expression of a new genetic programme

31
Q

What are examples of metaplasia

A

Smoking changes bronchial pseudostratified ciliated epithelium to stratified squamous non- ciliated epithelium
Barrett’s oesophagus - stratified squamous epithelium becomes gastric glandular epithelium with persistent acid reflux
Damage to bone marrow allows spleen to undergo metaplasia to become bone marrow and produce blood cells
Fibroblasts undergo metaplasia to produce osteoblasts, which produces bone in muscle after trauma

32
Q

What is metaplasia a prelude to cancer

A

Epithelial metaplasia

eg. Barrett’s epithelium, intestinal metaplasia of the stomach

33
Q

Describe aplasia

A

Complete failure of a specific tissue or organ to develop
Embryonic developmental disorder
Eg. Thymic aplasia (infections and autoimmune problems), aplasia of a kidney
Also used to describe an organ whose cells have ceased to proliferate
Eg. Aplasia of bone marrow in aplastic anaemia

34
Q

What is hypoplasia and give an example

A

Underdevelopment or incomplete development of tissue or organ at embryonic stage (inadequate number of cells)
Eg. Renal, breast, testicular in Klinefelter’s syndrome, chambers of heart

35
Q

What is involution and give an example

A

Normal programmed shrinkage of an organ

Eg. Uterus after childbirth, thymus in early life

36
Q

What is reconstitution and give an example

A

Replacement of a loss part of the body

Eg. Lizard tail, deer antlers, finger after clean cut in infant

37
Q

What is atresia and give an example

A

Congenital imperforation of an opening

Eg. Anus, vagina, small bowel

38
Q

What is dysplasia

A

Abnormal maturation of cells within tissue
Potentially reversible
Often pre-cancerous condition

39
Q

Left ventricle hypertrophy causes, complications

A

Causes - hypertension, aortic valve stenosis

Complications - heart failure, arrhythmia, MI, atrial fibrillation, sudden cardiac arrest

40
Q

Barrett’s oesophagus description, cause, complication

A

Stratified squamous epithelium becomes gastric glandular (simple columnar goblet cell) epithelium with persistent acid reflux
Complication - oesophageal adenocarcinoma

41
Q

Traumatic myositis ossificans description

A

Calcification of large muscles due to metaplasia of fibroblasts to osteoblasts due to trauma
Occurs in premature return to activity before proper healing
Often disappears through reverse metaplasia

42
Q

Benign prostatic hyperplasia macroscopic appearance, complications

A

Enlargement of prostate gland pushes against urethra and bladder
Complications - urinary retention (sudden inability to urinate), bladder hypertrophy, UTI, bladder stones, bladder damage

43
Q

Psoriasis presentation, macroscopic and microscopic appearance, pathophysiology

A

Presentation - patches of red inflamed skin, pain, itchiness, yellow nail colour or detach, scalp problems
Microscopic - neutrophils in epidermis, thinning of epidermis, vessels close to epidermis, thickening of skin (hyperkeratosis)
Macroscopic - raised red plaques covered with white scales
Pathophysiology - trigger (infection, trauma) causes recruitment of WBC to dermis and epidermis resulting in plaques
Activated T-cells cause keratinocyte proliferation through growth factor production
Production of cytokines and other mediators (TNF-a) cause inflammation