Chapter 2 Flashcards
What is the mechanism of hypertrophy (increase in the size of the cells)?
Hypertrophy is a result of increased cellular protein production
What causes most forms of pathological hyperplasia?
Excessive of inappropriate actions of hormones on growth factors acting on target cells
e.g endometrial hyperplasia due to hormone induced hyperplasia
What is atrophy?
Atrophy is a reduction in the size of an organ or tissue due to a decrease in cell size and number
What are 6 causes of atrophy?
- Decreased workload (disuse atrophy)
- Loss of innervation (denervation atrophy)
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrine stimulation
- Pressure
What is the main pathway of degradation of cellular proteins involved in atrophy?
Ubiquitin-proteasome pathway
What is a residual body, and what is an example?
Membrane-bound cell debris within autophagic vacoules that has resisted digestion and persisted in the cystoplasm
e.g. lipofuscin granules
What is the most common epithelial metaplasia?
Columnar to squamous
What is metaplasia and in which cell types can it occur?
Reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type
What type of metaplasia occurs in Barretts oesophagus?
Squamous epithelium → intestinal-like columnar cells under the influence of refluxed gastric acid
- predisposes to adenocarcinomas
What is myositis ossificans?
A form of connective tissue metaplasia where bone forms in muscle
How does metaplasia occur – do existing cells change form?
- Does not result from a change in the phenotype of an already differentiated cell type
- results from either reprogramming of local tissue stem cells, or
- colonisation by differentiated cell populations from adjacent sites
What are the three patterns of nuclear change seen in necrosis?
Karyolysis (basophilia of the chromatin may fade)
Pyknosis (nuclear shrinkage and increased basophilia)
Karyorrhexis (pynokic nucleus undergoes fragmentation)
3 major consequences of mitochondrial damage?
- ATP depletion
- Generation or reactive oxygen species
- Leakage of proteins (due to channel formation by action of BAX and BAK)
Chemical species that have a single unpaired electron in their outer orbit
Free radicals
Excessive intracellular calcium may cause cell injury by these two mechanisms
- opening of mitochondrial permeability transition pore → reduction ATP
- activation of enzymes which can cause cell damage (phospholipases, proteases, endonucleases, ATPases)
