Pathology: Necrosis and Apoptosis Flashcards

1
Q

Define hypertrophy

A

An increase in cell size

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2
Q

Define hyperplasia

A

An increase in cell numbers

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3
Q

Define atrophy

A

Reduction in cell size

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4
Q

Define hypoplasia

A

A below-normal number of cells

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5
Q

What factors overwhelm cell stress coping mechanisms such as hyperplasia and hypertrophy?

A
  • Rapidity of stress

- Quantity of stress

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6
Q

What are the 2 possible outcomes of the cell stress coping mechanisms being overwhelmed?

A
  • Apoptosis

- Necrosis

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7
Q

Describe necrosis

A
  • Requires no energy
  • Always pathological
  • Uncontrolled cell death
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8
Q

List the types of necrosis

A
  • Coagulative necrosis
  • Liquefactive necrosis
  • Caseous necrosis
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9
Q

Describe coagulative necrosis

A
  • The cell outline is preserved
  • So the tissue still has some structure
  • Common with hypoxic, ischemic/infarction injury
  • Cells are consumed by enzymes
  • Doesn’t occur in the brain
  • Cell is NOT destroyed by proteolysis via its enzymes
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10
Q

What kinds of injury commonly causes coagulative necrosis?

A
  • Hypoxic

- Ischemic, infarctions

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11
Q

Describe liquefactive necrosis

A
  • Cells form a liquid (no cell structure remains)
  • Pus
  • Associated with localised bacterial/fungal infections
  • Brain necrosis is liquefactive
  • After/if pus clears leaves a cavity
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12
Q

Describe caseous necrosis

A
  • Cheesy necrosis
  • Granulomatous inflammation with central necrosis
  • Associated with TB
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13
Q

Define apoptosis

A

Programmed cell death in response to specific signals

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14
Q

Describe apoptosis

A
  • Requires energy
  • Can be physiological or pathological
  • Can be triggered by intrinsic or extrinsic factors
  • Mechanism relies on caspase cascade
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15
Q

Give examples of pathological apoptosis

A
  • Some autoimmune disorders
  • Infective disease
  • Cancer
  • In response to trauma
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16
Q

Give an example of physiological apoptisis

A
  • Growth and development
    e. g. finger development
  • Removal of self-reactive lymphocytes
  • Involution of the uterus
17
Q

Describe the extrinsic pathway for apoptosis

A
  • Initiated by the activation of an death receptor (Fas or TNFR)
  • The fas receptor is activated by a fas ligand on another cell (often a type of T-Lymphocyte)
    OR
  • The TNF receptor (TNFR) can is activated by TNF
  • Both mechanisms are mediated by fas associated death domain (FADD)
  • Causes a caspase cascade
18
Q

Describe the mitochondrial mechanism for the intrinsic pathway for apoptosis

A
  • Normally cell survival signals promote anti-apoptotic molecules in the mitochondrial membrane
  • These inhibit Bax, Bak
  • When the signals stop the Bax is free to form channels in the membrane allowing the contents to escape
  • Cytochrome C escapes
19
Q

Describe the role p53 plays in apoptosis

A
  • Involved at cell cycle checkpoints
  • Checks for errors in DNA
  • If error found, repair is attempted
  • If it fails then apoptosis is induced
20
Q

List the risks of not having enough apoptosis

A
  • Cancer

- Autoimmune disease

21
Q

List the risks of having too much apoptosis

A
  • Neurodegenerative disorders

-

22
Q

Describe the morphological changes that occur during apoptosis

A
  • Cell shrinks
  • Pyknosis (irreversible chromatin condensation)
  • Nucleus breaks up
  • Apoptotic blebs form
  • Apoptotic bodies (blebs after they break off)
23
Q

What cell type phagocytose apoptotic bodies?

A

Macrophages

24
Q

What are the causes of cellular aging

A
  • Oxidative stress

- Accumulation of metabolic by-products