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Block 1 > Cellular Adaptations and Cellular Damage > Flashcards

Cellular Adaptations and Cellular Damage Flashcards

1
Q

Define cell adaptation

A

Reversible changes in cells due to changes in environment (pathological or physiological) Changes can be in number, size or type of cell

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2
Q

What are the 3 types of cells in terms of proliferative capacity?

A

Labile cells: continuously divide in adult life e.g. skin

Stable cells: infrequently divide but can divide rapidly if needed e.g. bone

Permanent cells: Never divide in adult life e.g. brain tissue

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3
Q

What are the 4 types of cellular adaptation?

A

Hypertrophy

Hyperplasia

Metaplasia

Atrophy

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4
Q

Define hyperplasia

What type of cells does this occur in?

Give some examples of tissues this can occur in

A

Increase in the number of cells within a tissue (labile or stable cells)

Reversible

  • Hormonal= endometrium during menstrual cycle
  • Compensatory= e.g. liver after partial hepatectomy
  • Pathological= e.g. chronic irritation, excessive growth factor stimulation
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5
Q

Define hypertrophy

A

Increase in cell size (increase in size of structural proteins)

Can occur in any cells, common in:

  • Permanent cells experiencing increased demand e.g.
    • Skeletal muscle
    • Uterine muscle in pregnancy
    • Pathological: e.g. cardiac muscle
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6
Q

Define atrophy

A
  • Reduction in cell size due to a loss of cell substance
  • Involves self digestion of organelles (autophagy)
    • e.g. ageing (brain), reduced workload, reduced blood supply
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7
Q

Define metaplasia

A
  • Reversible change of one mature adult cell type to another
  • Adaptive response
  • Usually involves epithelium

E.g.

  • Normal: Glandular to squamous epithelium in development of cervix
  • Pathological: oesophageal mucosa squamous to columnar epithelium in reflux oesophagitis (Barrett’s oesophagus)
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8
Q

What are the types of abnormal cell growth?

A

Dysplasia

Neoplasia

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9
Q

Define agenesis

A

Failure of differentiation into organ-specific tissue

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10
Q

Define dysplasia

A

Premalignant condition, occurs in labile tissues

  • Increased cell growth
  • Affects epithelia (e.g. cervix, bladder, stomach)
  • Altered differentiation
  • Cells mutate in a way that is not recognised by the cells’ regulatory mechanisms
  • Can acquire new mutations and become cancerous
  • Type of neoplasia
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11
Q

Define neoplasia

A

Abnormal growth of cells that persists after the stimulus has been removed

Cell growth escapes normal regulatory mechanisms:

  • Benign
  • Malignant- invasion and metastases
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12
Q

Define cell injury

A

Stimulus affecting cell has overwhelmed its capacity to adapt

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13
Q

What can cause cell injury and/or death?

A
  • Hypoxia
  • Physical agents (e.g. trauma, heat, cold)
  • Chemicals and drugs
  • Infection
  • Immune reactions (e.g. autoimmune, hyper-sensitivity or immunodeficient)
  • Genetic derangements
  • Nutritional imbalances (excess of insufficiency)
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14
Q

Why is ischaemia worse than hypoxia?

A

Hypoxia is oxygen deprivation (e.g altitude, anaemia)

Ischaemia is oxygen deprivation as well as lack of nutrients; build up of toxins occurs so cell injury is quicker and more severe (e.g. blockage of blood vessel)

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15
Q

What are the most common mechanisms of chemical injury to cells?

A
  • Damage to the osmotic environment
  • Biochemical cell reactions, e.g. lack of ATP
  • Damage to integrity of cell membrane
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16
Q

What is Marasmus?

A

Inadequate calorie intake resulting of metabolism of body tissues, e.g. skeletal muscle

17
Q

What is Kwashiorkor?

A

Adequate calorie intake but inadequate protein intake

  • protein stores in liver depleted
  • Liver’s ability to produce proteins is lost
    • e.g. albumin, loss of oncotic pressure of blood
18
Q

How does depletion of ATP cause damage to cells?

A

Loss of oxidative phosphorylation in mitochondria =

  • Loss of Na+ pump→influx of Na+ & Ca2+, efflux of K+→cellular swelling
  • Anaerobic glycolysis →acidosis
  • Detachment of ribosomes→decreased protein synthesis
19
Q

What can be caused by damage to the mitochondria?

A

Depletion of ATP

Generation of reactive oxygen species

Damage to mitochondrial membrane = membrane proteins released into cytosol causing cell apoptosis

20
Q

How can increased Ca2+ concentrations in cell cytoplasm cause damage?

A

Activates enzymes which break down cell membrane

Damage to DNA
ATP depletion

Can directly activate enzymes responsible for apoptosis

21
Q

What causes free radical production?

A

Absorption of radiant energy (e.g. UV light)

Enzymatic metabolism of chemicals (e.g. carbon tetrachloride)

Inflammation

22
Q

How are free radicals removed?

A

Antioxidants

Storage proteins (e.g. ferritin, transferrin)

Enzymes (e.g. catalase)

23
Q

How do free radicals cause damage?

A

Direct DNA strand damage

Interaction with proteins

Membrane lipid peroxidation→autocatalytic chain reaction

24
Q

What are the 2 types of cell death?

A

Necrosis

  • Always abnormal, pathological
  • Unregulated
  • Enzymatic cell digestion→ contents leak out

Apoptosis

  • Normal (pathological or physiological)
  • Internally controlled
  • Nuclear dissolution
25
Q

What are the different types of necrosis?

A
  • Coagulative:
    • Ischaemia
    • Cells die but substructure of tissue is maintained (e.g. kidney)
    • No enzymatic digestion of cells
  • Liquefactive:
    • Dead tissue replaced by liquid material
    • Enzymatic digestion of cells
    • Usually caused by inflammation, not usually ischaemic except in brain
  • Caseous: e.g. tuberculosis
  • Fat: Enzymes access and digest fat cells, e.g. pancreatitis
  • Infarction: Ischaemic necrosis due to reduced blood supply
    • White: blockage of arterial supply
    • Red: blockage of venous supply
26
Q

Give some examples of physiological and pathological apoptosis

A

Physiological:

  • Embyrogenesis
  • Involution of hormone dependent tissue
  • Cell loss in proliferative cell populations
  • Elimination of potentially harmful lymphocytes
  • Cells no longer required

Pathological:

  • Cells with DNA damage, or endoplasmic reticulum stress
  • Pathological atrophy if a duct is obstructed
  • Virus infected cells
27
Q

How does apoptosis occur?

A

Imbalance between anti-apoptotic and pro-apoptotic molecules in the cell

  • Activation of caspases
  • DNA and protein breakdown
  • Recognition by macrophages
28
Q

What disorders can be caused by dysregulated apoptosis?

A

Defective apoptosis with increased survival:

  • Autoimmune
  • Neoplastic

Defective apoptosis with decreased survival:

  • Ischaemic injury
  • Death of virus infected cells
29
Q
A

Block 1 (31 decks)

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