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
NECROSIS 1. describe the cellular changes 2. pattern of cell involvement 3. pathogenetic mechanisms 4. tissue reaction 5. physiological examples 6. pathological examples
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
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
27
For the following sites give the original cell type, the metaplastic cell type and the cause: 1. Bronchus 2. Lower oesophagus 3. Stomach
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
What are the consequences of metaplasia?
1. loss of normal function e.g. chest infections due to squamous metaplasia in bronchi 2. increased risk of malignancy
29
Describe the varied usage of the term dysplasia
- 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
Describe how dysplasia is a premalignant condition
- 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