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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
Q

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

A

Hypertrophy
Mechanical
Repair

26
Q

Types of increased growth

A

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
Q

Examples of normal physiological growth

A

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
Q

Example of increased growth - pathological

A

Left ventricle hypertrophy
Thyroid gland hyperplasia - graves
Cystic hyperplasia of the breast

29
Q

Pathological left ventricular hypertrophy

A

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
Q

Pathological thyroid hyperplasia - Graves’ disease

A

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
Q

Pathological cystic hyperplasia of the breast

A

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
Q

What is hypoplasia

A

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
Q

What is atrophy

A

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
Q

Factors maintaining normal cell integrity

A

Cell membrane
ATP generation (mitochondria)
Protein synthesis
Genetic apparatus

35
Q

Causes of cell injury

A

Hypoxia
Pro-inflammatory cytokines
Chemical toxins
Bacterial toxins

36
Q

Early reversible cell injury

A 
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
Q

Late irreversible cell injury

A 
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
Q

Morphological features of necrosis - late irreversible cell injury

A

Time - several hours to develop

Necrosis typically elicits an acute inflammatory reaction around 24 hours after cells death

39
Q

Apoptosis vs necrosis cellular changes

A

Apoptosis
Shrinkage
Fragmentation
(Apoptosis bodies)

Necrosis
Swelling
Coagulation or lytic changes

40
Q

Apoptosis vs necrosis

Pattern of cell involvement

A

Apoptosis
Single cell
Necrosis
Groups of cells

41
Q

Apoptosis vs necrosis

Pathogenetic mechanisms

A

Apoptosis
Energy dependent
Tightly regulated

Necrosis
Energy independent
Loss of cell integrity

42
Q

Apoptosis vs necrosis

Tissue reaction

A

Phagocytosis of apoptotic bodies
No inflammation

Necrosis
Inflammation

43
Q

Apoptosis vs necrosis

Physiological example

A

Apoptosis yes - normal cell turnover

Necrosis none

44
Q

Apoptosis vs necrosis

Pathological example

A

Apoptosis - yes

Necrosis- yes

45
Q

Types of abnormalities of cell differentiation

A

Metaplasia

Dysplasia

46
Q

Define metaplasia

A

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
Q

Examples of common metaplasia

A

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
Q

Consequences - metaplasia

A

Loss of normal cell function
E.g. Chest infections due to squamous metaplasia in bronchi
Increased risk of malignancy

49
Q

Definition of dysplasia

A

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
Q

Dysplasia as premalignant condition

A

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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