Lecture 2: Cell Injury, Adaptation, Death Flashcards
Etiology
Cause(s) of a condition
Pathology
Study of suffering, disease
Morphology
How pathology manifests cellularly; functional + clinical
Types of adaptive cell responses
- Hyperplasia
- Hypertrophy
- Atrophy
- Metaplasia
Atrophy examples
- Physiologic:
- Developmental regression - Pathologic:
- Disuse, denervation, ischemia, aging, pressure, wasting
Atrophy mechanisms
Lysosomes, ubiquitin proteasome paths, autophagic vacuoles, residual bodies
Metaplasia
When epithelia switches cell types
Cell injury
Occurs when adaptive response limits are exceeded
1. Reversible
2. Irreversible
3. Cell death
Threshold depends on cell state
Types of cell death
- Necrosis (always patho.)
- Apoptosis (physio/patho)
- Necroptosis
- Pyroptosis
- Ferroptosis
Subcellular alterations occur (IC accumulations, calcification, aging)
Etiologies of cell injury
- Hypoxia (ischemia)
- Chemicals
- Infections
- Immune cells
- Genes
- Nutrition, etc.
Common cell injury sites
- Mitochondria
- Cell membrane
- Nucleus
Aspects of mitochondrial injury
Dysfunction leads to widespread stress/injury; ROS
Necrosis
Gross, histologic cell death hallmark
Apoptosis
Programmed cell death
Necroptosis
RIPK3-programmed necrosis
Pyroptosis
Activation of cytoplasmic danger-sensing inflammasome complex
Anoikis
“Homelessness”
Apoptosis due to loss of ECM interactions
Necrosis characteristics
Enzymatic digestion + leakage of cell contents; coagulative/liquefactive manifestations; swelling
Apoptosis characteristics
- Single cell
- Nuclear fragmentation + cell shrinkage
- Non-inflammatory
- Membrane remains intact
Apoptosis 2 main pathways
- Intrinsic (mitochondria mediated)
- Extrinsic (cell signal mediated; executioner caspases)
Autophagy
Subcellular alterations in cell injury:
- Lysosomal catabolism
- Smooth ER induction (ribosome loss)
- Mitochondrial alteration
- Cytoskeletal abnormalities
Mallory bodies
Formed in alcoholic liver cirrhosis; minute hyaline droplets
Normal IC accumulations
Water, lipids, proteins
Abnormal IC accumulations
- Exogenous e.g. iron, copper
- Endogenous e.g. complex carbs
IC calcification
- Dystrophic (local, dying tissue)
- Metastatic (secondary to hypercalciemia)