Pathology - cells (including cell death) Flashcards

1
Q

Define autophagy

A

process for cells to remove organelles + denatures proteins

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2
Q

Define heterophagy

A

process of cell consuming material from its environment

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3
Q

Where is energy generated in a cell and what happens if this is damaged?

A

Mitochondria - ATP produced in intermembrane space by oxidative phosphorylation
Mitochondria also regulate programmed cell death (apoptosis)
If mitochondria damaged by toxins, decreased blood supply or trauma - ATP generation fails - cell dies by necrosis

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4
Q

What forms of mitochondrial disease are there?

A
X-linked = fathers cannot pass to sons
Autosomal = caused by autosomal gene abnormality
Maternally-inherited = mutation in mitochondrial DNA
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5
Q

What are growth factors?

A
  • promote entry of cells into cell cycle
  • remove block on cell cycle progression
  • prevent programmed cell death (apoptosis)
  • enhance synthesis of cell components (eg epiderm growth factor for skin wound healing)
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6
Q

Describe the cell cycle

A

G1 = cell preparing to divide - cell grows + copies organelles
S-phase (in interphase) = DNA replicated
G2 = cell continues to grow, centrosome replication completed
M-phase = mitotic phase = cell divides its copied DNA + cytoplasm to make 2 new cells (involves mitosis + cytokinesis)

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7
Q

Describe stem cells

A
  • have capacity for self-renewal

- asymmetric division (one daughter cell can mature while other remains stem cell)

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8
Q

Totipotent stem cell

A
  • embryonic

- can give rise to all types of differentiated/mature tissues

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9
Q

Adult/tissue stem cells

A

can only replace cells in tissues in which they reside

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10
Q

Multipotent stem cells

A
  • in bone marrow + fat

- can give rise to cartiocytes (cartilage cells), osteocytes, adepocytes (fat cells) + myocytes (muscle cells)

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11
Q

What are 4 cell adaptations

A
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
(reversible changes in size, number, phenotype, metabolic activity or functions of cells in response to changes in their environment)
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12
Q

Hypertrophy

A
  • increase in size of cells (increase in size of affected organ)
  • physiological or pathological
  • related to increased workload
    physiological = uterus in pregnancy
    pathological = myocardium in hypertension
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13
Q

Hyperplasia

A
  • increase in number of cells in organ/tissue in response to a stimulus
  • can only occur if cells can divide
  • can be physiological or pathological
  • can occur alongside hypertrophy
  • regresses if stimulus removed
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14
Q

Atrophy

A
  • decrease in size of organ/tissue due to decreases cell size + number
  • physiological or pathological
    eg disuse atrophy, denervation atrophy, pressure atrophy, inadequate nutrition
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15
Q

Metaplasia

A
  • reversible change in which one differentiated cell type is replaced by another cell type
  • adaptive response - replacement cell type better able to withstand adverse environment
  • caused by reprogramming of stem cells
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16
Q

What is necrosis?

A
  • accidental/unregulated cell death
  • always pathological
  • damage to cell membranes - lysosomal enzyme digestion of cell
  • leakage of cell contents - inflammatory reaction
17
Q

Mechanisms underlying necrosis

A
  • depletion of ATP
  • mitochondrial damage
  • influx of calcium
  • accumulation of oxygen-derived free radicals
  • membrane permeability defects
  • DNA + protein damage
18
Q

What is apoptosis?

A
  • programmed cell death
  • no inflammatory reaction
  • many normal functions
  • physiological (eg destruction of cells during embryogenesis) + pathological (eg viral infections)
19
Q

What are the 2 types of pathological calcification?

A
dystrophic = normal serum calcium, calcium deposited in dead/damaged tissue
Metastatic = hypercalcemia, increased PTH, increased bone turnover, vitamin D excess, sarcoidosis
20
Q

How are apoptotic cells removed?

A
  • phosphatidylserine flips from inner to outer aspect of cell membrane
  • recognised by macrophage receptors
  • apoptotic cells secrete soluble factors which recruit macrophages
  • apoptotic bodies get coated with thrombospondin or C1q which attracts macrophages
  • dead cells disappear within minutes