cellular adaptations, cell injury, cell death Flashcards
cell adaptations
-hyperplasia- increase in NUMBER of cells
-hypertrophy- increase in SIZE of cells
-metaplasia- reversible change in which one differentiated cell is replaced by another cell type
-atrophy- reduction in size of organ d/t decrease in cell SIZE and NUMBER
reversible injury vs irreversible injury
-reversible- cell injury
-irreversible- necrosis/apoptosis
cell death
-IRREVERSIBLE
-necrosis- denaturation of cell proteins, leakage, nucleus disintegrates
-apoptosis
-irreversible mitochondrial dysfunction = necrosis
-diff types:
-coagulative- solid organs, cellular outline maintained, nucleus dissolves (kidney, heart, liver)
-localized area of coagulative necrosis = infarct
-liquefactive- brain
-fatty- breast, any fat
-caseous- (cheese)- granulomas, e.g. tuberculosis
-gangrene- extremities, bowel, non-specific -> wet and dry
-fibrinoid- usually in vasculitis, rheumatioid non-specific
hypertrophy
-!!increase in SIZE of cells -> increase in size of the organ
-NO new cells, just larger cells
-increased cellular protein production
-*Cells able to divide may also undergo hyperplasia (increase number of cells)
-Permanent cells (striated muscle, nerve tissue, cardiac muscle) can only undergo hypertrophy
-types:
-physiologic- uterus during pregnancy
-pathological- heart secondary to aortic stenosis or HTN
hyperplasia
-INCREASE IN NUMBER OF CELLS
-Physiologic hyperplasia – increase in glandular epithelium of breast at puberty and pregnancy
-also with enlargement (hypertrophy) of the glandular epithelial cells
-Pathologic hyperplasia- excessive hormones or growth factors acting on target cells
-endometrial hyperplasia
atrophy is secondary to
-Decrease in size of cells
-secondary to:
-DECREASED WORKLOAD
-DENERVATION
-DECREASED BLOOD FLOW
-DECREASED NUTRITION
-AGING (involution)
-PRESSURE
metaplasia
-can lead to cancer
-Replacement of one differentiated (mature, adult) cell by another cell type
-Reversible, but if persists can lead to dysplasia
-MC is columnar to squamous
-Results from either:
-reprogramming of local tissue stem cells OR
-colonization by differentiated cell populations from adjacent sites
-Stimulated by signals generated by cytokines, growth factors, and ECM components in cells’ environment
-ex- columnar epithelium -> makes mucus to protect against acid -> squamous protects
metaplasia examples chart
-columnar epithelium - produces mucus to protect against acid
-squamous is protective
- Barrett’s esophagus
- Muscles in a body builder
- Enlarged heart from aortic stenosis
- Post-menopausal uterus lining
-A. Physiologic hypertrophy
-B. Pathologic hypertrophy
-C. Atrophy
-D. Metaplasia
-1. D
-2. A
-3. B
-4. C
-A. Physiologic hypertrophy
-B. Pathologic hypertrophy
-C. Atrophy
-D. Metaplasia
what causes cell injury/death
-1. Hypoxia: reducing aerobic oxidative respiration
-What causes hypoxia?
-reduced blood flow (ischemia)
-low oxygenation of blood from cardiorespiratory failure
-decreased oxygen-carrying capacity (anemia, carbon monoxide poisoning and severe blood loss)
-2. Physical Agents (temperature (burns and deep cold), sudden changes in atmospheric pressure, radiation, electric shock)
-Chemical Agents and Drugs
-Infectious Agents
-Immunologic Reactions
-Genetic Abnormalities
-Nutritional Imbalances
reversible changes
-Ischemia
-REDUCED oxidative phosphorylation
-ATP depletion/ loss or reduction of Na+/K+ pump.
-Cellular “SWELLING” -> edema
process of cell injury to cell death
-Damage to mitochondria -> decreased oxidative phosphorylation and ATP
-Reduced Na/K -> swelling (reversible)
-Increase anaerobic glycolysis -> Decrease in protein synthesis
-!!Failure of CA pump—-Ca enters cell causing membrane and nuclear damage by activating phospholipases, proteases, endonuclease, and ATPases
-Denaturation of intracellular proteins, enzymatic digestion of cell, contents leak out and elicit inflammation
-irreversible mitochondrial dysfunction = necrosis
!coagulative necorsis
-more common bc it happens in solid organs (anything with solid wall too)
-Cell outlines preserved -> but nucleus disappears!
-Increased eosinophilia (pink) seen at first because of denatured cytoplasmic proteins
-Local area of coagulative necrosis – infarct!
-Heart, kidney, solid organs
liquefactive necrosis
-brain
-Digestion of dead cells resulting in liquid, viscous mass
-Occurs in abscesses (bacteria)
-Neutrophils release lysosomal enzymes -> digest -> protein degradation
gangrene necrosis
-Not specific pattern of cell death, but term commonly used in clinical practice
-Ex: limb, generally lower leg, that has lost its blood supply and has undergone necrosis (typically coagulative necrosis) involving multiple tissue planes
-When its a bacterial infection -> more liquefactive necrosis because of degradative enzymes in bacteria and attracted leukocytes (wet gangrene)
apoptosis vs necrosis
-APOPTOSIS (“normal” death) -> NORMAL
-can be pathologic OR normal
-ATP needed
-membrane integrity sustained -> little leakage -> NO INFLAMMATION
-NECROSIS (“premature” or “untimely” death due to “causes”) -> PATHOLOGIC
-always pathologic
-no ATP
-leaks debris -> inflammation
-many cells involved in area
