Lecture 2: Cell Injury, Adaptation, Death Flashcards

1
Q

Etiology

A

Cause(s) of a condition

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2
Q

Pathology

A

Study of suffering, disease

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3
Q

Morphology

A

How pathology manifests cellularly; functional + clinical

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4
Q

Types of adaptive cell responses

A
  1. Hyperplasia
  2. Hypertrophy
  3. Atrophy
  4. Metaplasia
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5
Q

Atrophy examples

A
  1. Physiologic:
    - Developmental regression
  2. Pathologic:
    - Disuse, denervation, ischemia, aging, pressure, wasting
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6
Q

Atrophy mechanisms

A

Lysosomes, ubiquitin proteasome paths, autophagic vacuoles, residual bodies

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7
Q

Metaplasia

A

When epithelia switches cell types

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8
Q

Cell injury

A

Occurs when adaptive response limits are exceeded
1. Reversible
2. Irreversible
3. Cell death
Threshold depends on cell state

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9
Q

Types of cell death

A
  • Necrosis (always patho.)
  • Apoptosis (physio/patho)
  • Necroptosis
  • Pyroptosis
  • Ferroptosis
    Subcellular alterations occur (IC accumulations, calcification, aging)
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10
Q

Etiologies of cell injury

A
  • Hypoxia (ischemia)
  • Chemicals
  • Infections
  • Immune cells
  • Genes
  • Nutrition, etc.
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11
Q

Common cell injury sites

A
  • Mitochondria
  • Cell membrane
  • Nucleus
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12
Q

Aspects of mitochondrial injury

A

Dysfunction leads to widespread stress/injury; ROS

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13
Q

Necrosis

A

Gross, histologic cell death hallmark

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14
Q

Apoptosis

A

Programmed cell death

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15
Q

Necroptosis

A

RIPK3-programmed necrosis

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16
Q

Pyroptosis

A

Activation of cytoplasmic danger-sensing inflammasome complex

17
Q

Anoikis

A

“Homelessness”
Apoptosis due to loss of ECM interactions

18
Q

Necrosis characteristics

A

Enzymatic digestion + leakage of cell contents; coagulative/liquefactive manifestations; swelling

19
Q

Apoptosis characteristics

A
  • Single cell
  • Nuclear fragmentation + cell shrinkage
  • Non-inflammatory
  • Membrane remains intact
20
Q

Apoptosis 2 main pathways

A
  1. Intrinsic (mitochondria mediated)
  2. Extrinsic (cell signal mediated; executioner caspases)
21
Q

Autophagy

A

Subcellular alterations in cell injury:
- Lysosomal catabolism
- Smooth ER induction (ribosome loss)
- Mitochondrial alteration
- Cytoskeletal abnormalities

22
Q

Mallory bodies

A

Formed in alcoholic liver cirrhosis; minute hyaline droplets

23
Q

Normal IC accumulations

A

Water, lipids, proteins

24
Q

Abnormal IC accumulations

A
  • Exogenous e.g. iron, copper
  • Endogenous e.g. complex carbs
25
Q

IC calcification

A
  • Dystrophic (local, dying tissue)
  • Metastatic (secondary to hypercalciemia)