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Y3 > Cell Turnover And Disorders Of Cell Proliferation Amd Differentiation > Flashcards

Cell Turnover And Disorders Of Cell Proliferation Amd Differentiation Flashcards

1
Q

Basic differences in normal and abnormal cell growth and turnover

A

Normal cell turnover vs
Changes in cell growth (inc and Dec)
Cell death
Abnormalities of cell differentiation

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2
Q

Labile cell types of cell renewal

A

Steady state renewal

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3
Q

Stable cell type of cell renewal

A

Conditional cell renewal

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4
Q

Permanent cell type of cell renewal

A

Non replacing

So no renewal

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5
Q

Normal proliferative capacity of labile cells

A

High

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6
Q

Do labile cells have the capacity to inc proliferation

A

Yes

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7
Q

Normal proliferative activity of stable cells

A

Low

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8
Q

Is there capacity for increased proliferation

A

Yes

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9
Q

Normal proliferative activity of permanent cells

A

None

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10
Q

Is there Capacity for increased proliferation in permanent cells

A

No

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11
Q

Stem cells capacity to divide

A

Proliferative compartment so can divide and differentiate into different cell types

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12
Q

Transit cells state of cell division

A

Maturing cells

Limited capacity for division

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13
Q

Mature functional cells state of cell division.

A

Non dividing

Programmed to die and require replacement

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14
Q

When does the epidermis lose its capacity to divide

A

3 basic layers, basal, prickle, horny

At the prickle layer they lose their nuclei and capacity to divide

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15
Q

Phases of the cell cycle what they are called and what happens at each

A

G0 - quiescent phases not dividing can move to dividing G1 with the right signals
G1 - gap1 (pre-synthetic) growth phase
S - synthetic replication DNA
G2 - gap 2 (pre-mitotic) more growth
M - mitotic cell division
At the G1 phase - the cell can become terminally differentiated or go through the cell cycle again

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16
Q

Factors which control cell division

A

Polypeptide growth factors and cytokines
Cyclins
Inhibitory factors

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17
Q

What do polypeptide growth factors and cytokines do

A

Act on receptors on the cell surface
Formation of second messenger in cytoplasm
DNA synthesis in the nucleus

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18
Q

What do cyclins do to control the cell cycle

A

Activate proteins involved in DNA replication and other events on the cell cycle

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19
Q

What are the inhibitor factors which control cell division

A

Polypeptide growth factors/cytokines
Tumour suppressor genes p53
Cyclin dependent kinase inhibitors p21,27

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20
Q

Patterns of increased growth - normal

A

Inc number of the cells
Inc the size of the cells
Occurs as a result of increased demand for function
Stimuli may be mechanical, chemical or hormonal
Capacity for cell division governs the pattern of inc growth (and also response to cell loss)

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21
Q

Inc in no of cells is called

What is the stimuli for this

A

Hyperplasia

Stimulus normal or chemical

22
Q

Inc in size of cells called and stimulus for this

A

Hypertrophy

Mechanical stimuli usually

23
Q

What is the response of labile cells to increased demand for function
Hypertrophy or hyperplasia and the stimulus and response to injury this action causes

A

Hyperplasia
Chemical or hormonal
Regeneration

24
Q

What is the response of stable cells to increased demand for function
Hypertrophy or hyperplasia and the stimulus and response to injury this action causes

A

Hyperplasia
Chemical or hormonal
Regeneration

25
What is the response of permanent cells to increased demand for function Hypertrophy or hyperplasia and the stimulus and response to injury this action causes
Hypertrophy Mechanical Repair
26
Types of increased growth
Physiological - changes largely reversible if the stimulus causing them is removed Pathological - changes less readily reversible If excessive growth persists may predispose to neoplastic transformation
27
Examples of normal physiological growth
Pregnancy - uterus - myometrial hypertrophy and hyperplasia due to mechanical factors and oestrogen Breast - glandular hyperplasia due to oestrogen and progesterone Skeletal muscle - hypertrophy in athletes Bone marrow - hyperplasia of erythroid cells in response to blood loss
28
Example of increased growth - pathological
Left ventricle hypertrophy Thyroid gland hyperplasia - graves Cystic hyperplasia of the breast
29
Pathological left ventricular hypertrophy
Causes - Systemic hypertension Aortic value disease (aortic stenosis or incompetence) Mitral incompetence Coronary artery atheroma Consequences Initially compensates for increased demand Later leads to cardiac failure (myocardial ischaemia may also occur)
30
Pathological thyroid hyperplasia - Graves' disease
Hyperplasia of thyroid gland with increased production of thyroxine (thyrotoxicosis) Due to production of thyroid stimulating auto antibodies act on same receptors as TSH Not susceptible to normal negative feedback mechanism
31
Pathological cystic hyperplasia of the breast
Proliferation of glandular elements with formation of cysts Probably due to hormonal factors - occurs in women between menarche and menopause - normal variations in breast tissue during the menstrual cycle
32
What is hypoplasia
Failure of a tissue or organ to reach normal size during development Causes include: genetic defects, intrauterine infection, toxic insults - limbs in thalidomide effected people
33
What is atrophy
Decrease in size of tissue or organ at a stage after initial development Dec cell size or number Can be physiological - post puberty decline in thymus size Part of normal ageing process Causes of pathological atrophy - Loss of hormonal stimulation e.g. Atrophy of endocrine organs secondary to pituitary disease Dec workload - disuse atrophy of muscle Loss of innervation
34
Factors maintaining normal cell integrity
Cell membrane ATP generation (mitochondria) Protein synthesis Genetic apparatus
35
Causes of cell injury
Hypoxia Pro-inflammatory cytokines Chemical toxins Bacterial toxins
36
Early reversible cell injury
``` Associated with swelling Factors involved - entry of sodium and water into cell (membrane dysfunction) - mitochondrial swelling - dilatation of endoplasmic reticulum morphological terms - hydropic change - vacuoles degeneration - ballooning degeneration ```
37
Late irreversible cell injury
``` Necrosis Nuclear changes -shrinkage (pyknosis) - Fragmentation (karyorrhexis) - disappearance (karyolysis) Cytoplasmic changes - denaturation of proteins -- inc cytoplasmic eosinophilia (coagulation necrosis) - acid liking staining cytoplasm - cell outlines still visible -- occurs in hypoxic/ischaemic injury - enzymatic digestion of the cell -- disappearance of cells (lyric necrosis) -- more common with cytokines mediated injury e.g. Acute viral hepatitis ```
38
Morphological features of necrosis - late irreversible cell injury
Time - several hours to develop | Necrosis typically elicits an acute inflammatory reaction around 24 hours after cells death
39
Apoptosis vs necrosis cellular changes
Apoptosis Shrinkage Fragmentation (Apoptosis bodies) Necrosis Swelling Coagulation or lytic changes
40
Apoptosis vs necrosis | Pattern of cell involvement
Apoptosis Single cell Necrosis Groups of cells
41
Apoptosis vs necrosis | Pathogenetic mechanisms
Apoptosis Energy dependent Tightly regulated Necrosis Energy independent Loss of cell integrity
42
Apoptosis vs necrosis | Tissue reaction
Phagocytosis of apoptotic bodies No inflammation Necrosis Inflammation
43
Apoptosis vs necrosis | Physiological example
Apoptosis yes - normal cell turnover | Necrosis none
44
Apoptosis vs necrosis | Pathological example
Apoptosis - yes | Necrosis- yes
45
Types of abnormalities of cell differentiation
Metaplasia | Dysplasia
46
Define metaplasia
Replacement (potentially reversible) of one differentiated cell type by another differentiated cell type Usually occurs as response to unfavourable environment for the original cell type Barrett's oesophagus
47
Examples of common metaplasia
Site - bronchus Original cell type - ciliated columnar (resp epithelium) Metaplastic cell type - squamous Cause - cigarette smoking Site - lower oesophagus (Barrett's) Original cell type - squamous Metaplastic cell type - gastric (columnar lined distal oesophagus) Cause - acid reflux Site - stomach Original cell type - columnar (gastric) Metaplastic cell type - intestinal Cause - chronic inflammation- H pylori infection
48
Consequences - metaplasia
Loss of normal cell function E.g. Chest infections due to squamous metaplasia in bronchi Increased risk of malignancy
49
Definition of dysplasia
Literally 'disordered development' Controversial term due to varied usage: - developmental abnormalities -e.g. Cystic renal dysplasia - tumour like malformation-e.g. Fibrous dysplasia of bone - premalignant changes (usually epithelial) E.g. Epithelial dysplasia in UC
50
Dysplasia as premalignant condition
Changes resemble those sent in neoplastic cells Not yet invasive, but potential for progression to invasive carcinoma if untreated Increasing grades of dysplasia described (mild, moderate, severe) - potential for reversibility diminishes with progression in grade - severe dysplasia = carcinoma in situ Intraepithelial neoplasia now preferred term in many situations -e.g. Cervical intraepithelial neoplasia or CIN: CIN grade 1 mild neoplasia, CIN 2 = moderate dysplasia, CIN 3 = severe dysplasia - basis for screening

Y3 (22 decks)

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