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Year 3 Lecture Content > Cell Turnover and Disorders of Cell Proliferation and Differentiation > Flashcards

Cell Turnover and Disorders of Cell Proliferation and Differentiation Flashcards

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3
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What are the factors controlling cell division

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Polypeptide Growth Factors and Cytokines

  • act on receptors on cell surface
  • formation of second messenger in cytoplasm
  • DNA synthesis in nucleus

Cyclins

• activate proteins involved in DNA replication and other events in cell cycle

Inhibitory Factors

  • polypeptide growth factors/cytokines
  • Tumour suppressor genes (e.g. p53)
  • Cyclin –dependent kinase inhibitors (e.g. p21, p27)
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4
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What pathways contol cell growth and differentiation?

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5
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Patterns of Increased Growth (excluding neoplasia) General Principles

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Increased growth can be due to an increase in NUMBER or SIZE of cells

  • Usually occurs as a result of INCREASED DEMAND FOR FUNCTION
  • Stimuli may be MECHANICAL, CHEMICAL or HORMONAL
  • Capacity for cell division governs the pattern of increased growth (and also response to cell loss)
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6
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Patterns of Increased Growth (excluding neoplasia) Two main types are?

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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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What are physiological changes that causes increased growth>?

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Physiological

– changes largely reversible if the stimulus causing them is removed.

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9
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Examples of Increased Growth - Pathological

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  1. Left ventricular hypertrophy
  2. Thyroid gland hyperplasia (Graves disease)
  3. Cystic hyperplasia of the breast
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10
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Left ventricular hypertrophy

What are the causes and consequences?

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Causes

  • Systemic hypertension
  • Aortic valve 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)
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11
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What problems does bicuspid aortic valves cause?

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bicuspid aortic valve -> aortic stenosis -> infective endocarditis

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12
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What happened to these thyroid tissues?

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Grave’s disease

Hyperplasia of thyroid gland with increased production of thyroxine (thyrotoxicosis)

  • Due to production of thyroid stimulating autoantibodies (immunoglobulins) which act on same receptors as thyroid stimulating hormone
  • Not susceptible to normal negative feedback mechanism
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13
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What happened to this breast lobule?

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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 menstrual cycle
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14
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What is hypoplasia

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Hypoplasia (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. hypoplastic limbs related to thalidomide
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15
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What is atrophy?

What are the causes of pathological atrophy?

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Decrease in size of tissue or organ at a stage after initial development

  • May be due to a decrease in cell size or number (i.e. opposite of hyperplasia and hypertrophy)
  • Can be physiological (e.g. post-pubertal atrophy of thymus gland)
  • Part of “normal” ageing process
  • Causes of pathological atrophy include:

– 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

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16
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Factors maintaining normal cell integrity

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Cell membrane

  • ATP generation (mitochondria)
  • Protein synthesis
  • Genetic apparatus
17
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What causes cell injury?

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Hypoxia

Pro-inflammatory cytokines

  • Chemical toxins
  • Bacterial toxins
18
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Early (Reversible) Cell Injury

What are the factors involved?

What are morphological terms?

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Typically associated with cell swelling

  • Factors involved – Entry of sodium and water into cell (membrane dysfunction) – Mitochondrial swelling – Dilatation of endoplasmic reticulum
  • Morphological terms

– Hydropic change - water in cells

– Vacuolar degeneration - loss of cytoplasmic

– Ballooning degeneration

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What can you see that is wrong in this hepatocyte?

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Hepatocyte Ballooning

Mallory’s Hyaline - globular red hyaline within hepatocytes - intermediate filament breaking down after chronic damage

20
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Late (Irreversible) Cell Injury leads to ______

Nuclear changes causing:

  • Pyknosis
  • karyorrehexis

Karyolysis

what cytoplasmic changes occur?

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Nuclear Changes

  • Shrinkage (pyknosis)
  • Fragmentaion (karyorrhexis)
  • Disappearance (karyolysis)

Cytoplasmic changes

• Denaturation of proteins

– Increased cytoplasmic eosinophilia (Coagulative necrosis)

– Typically occurs in hypoxic/ischaemic injury e.g. myocardial infarction

• Enzymatic digestion of cell

– Disappearance of cells (Lytic necrosis)

– More common with cytokine-mediated injury e.g. acute viral hepatitis

21
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Late (Irreversible) Cell Injury leads to ______

Nuclear changes causing:

  • Pyknosis
  • karyorrehexis

Karyolysis

what cytoplasmic changes occur?

A

Nuclear Changes

  • Shrinkage (pyknosis)
  • Fragmentaion (karyorrhexis)
  • Disappearance (karyolysis)

Cytoplasmic changes

• Denaturation of proteins

– Increased cytoplasmic eosinophilia (Coagulative necrosis)

– Typically occurs in hypoxic/ischaemic injury e.g. myocardial infarction

• Enzymatic digestion of cell

– Disappearance of cells (Lytic necrosis)

– More common with cytokine-mediated injury e.g. acute viral hepatitis

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Label this

A
23
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1) How long does it take for histological features of MI to be apparent?
2) Necrosis causes an acute inflammatory reaction which begins around how long after cell death?

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1) 4-12 hours after irreversible injury has occured
2) 24 hours after cell death

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What has happened to this myocardium after infarction

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25
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What changes are seen here with someone with acute hepatitis

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Confluent Centrilobular Necrosis (lytic pattern – cell outlines no longer visible)

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27
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What causes apoptosis to be signalled?

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28
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What can be seen here with a person with acute hepatitis

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Acidophil Body

29
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Define metaplasia

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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.

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31
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What are the consequences of metaplasia?

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  1. Loss of normal cell function e.g. chest infections due to squamous metaplasia in bronchi
  2. Increased risk of malignancy
32
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What happenes to this normal bronchial mucosa?

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Squamous Metaplasia (+ dysplasia)

33
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Dysplasia - Definition

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Literally ‘disordered development’

Controversial term due to varied usage:

  • Developmental abnormalities – e.g. cystic renal dysplasia
  • Tumour like malformations – e.g. fibrous dysplasia of bone
  • Premalignant changes (usually epithelial) – e.g. epithelial dysplasia in ulcerative colitis
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Dysplasia as a Premalignant Condition

Why is that?

What happnes in severe dysplacia?

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  • Changes resemble those seen 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 dysplasia, CIN 2 = moderate dysplasia, CIN 3 = severe dysplasia • Basis for screening
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Year 3 Lecture Content (33 decks)

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