Cell Turnover and Disorders of Cell Proliferation and Differentiation Flashcards

1
Q

Labile cells

  • Describe them in a few words
  • What is their normal level of proliferative activity?
  • Do they have capacity for increased proliferation?
  • Give examples
A
  • steady state renewal
  • high
  • yes
  • surface epithelia e.g. skin, gut, haemopoietic cells
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2
Q

Stable cells

  • Describe them in a few words
  • What is their normal level of proliferative activity?
  • Do they have capacity for increased proliferation?
  • Give examples
A
  • conditional renewal
  • low
  • yes
  • parenchymal cells of glandular organs e.g. liver, kidney, thyroid
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3
Q

Permanent cells

  • Describe them in a few words
  • What is their normal level of proliferative activity?
  • Do they have capacity for increased proliferation?
  • Give examples
A
  • non-replacing
  • none
  • no
  • neurones, cardiac muscle, skeletal muscle
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4
Q

Describe the states of cell division of

  • stem cells
  • transit cells
  • mature functional cells
A

Stem cells = proliferative compartment
Transit cells = maturing cells, limited capacity for division
Mature functional cells = non dividing, programmed to die and require replacement

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5
Q
  • Increased growth can be due to an increase in ……….. or ……… of cells
  • Usually occurs as a result of ……. ……. ….. …….
  • Stimuli may be ………….. , ………….. or ………..
  • Capacity for cell division governs the patter of increased growth (and response to cell loss)
A
  • Increased growth can be due to an increase in NUMBER or SIZE of cells
  • Usually occurs as a result of INCREASED DEMAND FOR GROWTH
  • Stimuli may be CHEMICAL, MECHANICAL or HORMONAL
  • Capacity for cell division governs the patter of increased growth (and response to cell loss)
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6
Q

What are the two main patterns of increased growth>

A

hyperplasia and hypertrophy

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7
Q

What is the difference between hypertrophy and hyperplasia?

How are their stimuli different?

A
Hyperplasia 
- increase in number of cells 
- stimulus is usually hormonal or chemical 
Hypertrophy 
- increase in size of cells 
- stimulus is usually mechanical
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8
Q

Do the following cells respond with hyperplasia or hypertrophy?

  • labile
  • stable
  • permanent
A
Labile 
- hyperplasia 
Stable 
- hyperplasia 
Permeneant 
- hypertrophy
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9
Q

How are pathological and physiological increased growth different?

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

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10
Q

Give 3 examples of physiological increased growth

A
  1. Pregnancy
    - uterus - myocetrial hypertrophy and hyperplasia due to mechanical factors and oestrogen
    - breast - glandular hyperplasia due to oestrogen and progesterone
  2. Skeletal muscle
    - hypertrophy ocurrido in athletes
  3. Bone marrow
    - hyperplasia of erythroid cells in response to blood loss
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11
Q

Give 3 examples of pathological increased growth

A
  1. left ventricular hypertrophy
  2. thyroid gland hyperplasia (Graves disease)
  3. cystic hyperplasia of the breast
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12
Q

What are the causes of left ventricular hypertrophy?

A
  • systemic hypertension
  • aortic valve disease (aortic stenosis or incompetence)
  • mitral incompetence
  • coronary artery atheroma (loss of some fibres so other fibres enlarge)
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13
Q

What are the consequences of left ventricular hypertrophy?

A
  • initially compensates for increased demand

- later leads to cardiac failure (myocardial ischaemia may also occur)

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14
Q

What is graves disease and what is the cause?

A
  • hyperplasia of the thyroid gland with increased prodcitin of thyroxine (thyrotoxicosis)
  • due to production of thyroid stimulating autoantibodies (Ig’s) which act on same receptors as thyroid stimulating hormone
  • not susceptible to normal negative feedback mechanism
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15
Q

What is 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 variation in breast tissue during menstrual cycle
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16
Q

What is hypoplasia?

What are the causes?

A

NOT the opposite of hyperplasia

  • failure of a tissue or organ to reach normal size during development
  • causes include genetic defects, intrauterine infection, toxic insults e.g. hypo plastic limbs related to thalidomide
17
Q

What is atrophy>

A
  • decrease in size of tissue or organ at a stage after initial development
  • may be due to decrease in cell size or number
  • can be physiological e.g. thymic atrophy
  • part of ‘normal’ ageing process
18
Q

What are the pathological causes of atrophy?

A
  • loss of hormonal stimulation e.g. atrophy of endocrine organs secondary to pituitary disease
  • reduction in blood supply
  • decreased workload e.g. disuse atrophy of muscle
  • loss of innervation
19
Q

What 4 factors maintain normal cell integrity?

A
  • cell membrane
  • ATP generation
  • protein synthesis
  • genetic apparatus
20
Q

What are the 4 causes of cell injury?

A
  • hypoxia
  • pro-inflammatory cytokines
  • chemical toxins
  • bacterial toxins
21
Q

What factors are involved in early (reversible) cell injury?

Give some morphological terms

A
Typically associated with cell swelling 
Factors involved 
- entry of Na+ and water into cell (membrane dysfunction)
- mitochondrial swelling 
- dilation of endoplasmic reticulum 
Morphological terms 
- hydropic change 
- vacuolar degeneration 
- ballooning degeneration
22
Q

What is the word for late (irreversible) cell injury?

Describe the nuclear changes in later (irreversible) cell injury.

A
NECROSIS 
Nuclear changes 
- shrinkage (pynknosis)
- fragmentation (karyorrhexis)
- disappearance (karyolysis)
23
Q

Describe the cytoplasmic changes seen in necrosis

A

Denaturation of proteins
- increased cytoplasmic eosinophilia (coagulative necrosis)
- typically occurs in hypoxic/ischaemic injury e.g. MI
Enzymatic digestion of cell
- disappearance of cells (lytic necrosis)
- more common with cytokine-mediated injury e.g. acute viral hepatitis

24
Q

APOPTOSIS

  1. describe the cellular changes
  2. pattern of cell involvement
  3. pathogenetic mechanisms
  4. tissue reaction
  5. physiological examples
  6. pathological examples
A

APOPTOSIS

  1. describe the cellular changes
    - shrinkage, fragmentation (apoptotic bodies)
  2. pattern of cell involvement
    - single cells
  3. pathogenetic mechanisms
    - energy dependent, tightly regulated
  4. tissue reaction
    - phagocytosis of apoptotic bodies, no inflammation
  5. physiological examples
    - UES, normal cell turnover, organ development
  6. pathological examples
    - Yes, including same factors as those cause necrosis
25
Q

NECROSIS

  1. describe the cellular changes
  2. pattern of cell involvement
  3. pathogenetic mechanisms
  4. tissue reaction
  5. physiological examples
  6. pathological examples
A

NECROSIS

  1. describe the cellular changes
    - swelling, coagulative or lytic damage
  2. pattern of cell involvement
    - groups of cells
  3. pathogenetic mechanisms
    - energy-independent
    - loss of cell integrity
  4. tissue reaction
    - inflammation
  5. physiological examples
    - No
  6. pathological examples
    - Yes
26
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
27
Q

For the following sites give the original cell type, the metaplastic cell type and the cause:

  1. Bronchus
  2. Lower oesophagus
  3. Stomach
A
  1. Bronchus
    - ciliated columnar
    - squamous
    - cigarette smoking
  2. Lower oesophagus
    - squamous
    - gastric
    - acid reflux
  3. Stomach
    - columnar
    - intestinal
    - chronic inflammation e.g. H.pylori infection
28
Q

What are the consequences of metaplasia?

A
  1. loss of normal function e.g. chest infections due to squamous metaplasia in bronchi
  2. increased risk of malignancy
29
Q

Describe the varied usage of the term dysplasia

A
  • literally means disordered development
    Developmental abnormalities
    e.g. cystic renal dysplasia
    Tumour like malformations
  • fibbers dysplasia of bone
    Premalignant changes (usually epithelial)
    e.g. epithelial dysplasia in UC
30
Q

Describe how dysplasia is a premalignant condition

A
  • changes resemble those seen in neoplastic cells
  • not yet invasive, but potential for precession to invasive carcinoma if untreated
  • increasing grads of dysplasia described (mild, moderate, severe)
  • potential for reversibility dimness with progression in grade
  • severe dysplasia = carcinoma in situ
  • intraepithelial neoplasia now preferred term in many situations e.g. cervical intraepithelial neoplasm or CIN
  • basis for screening