Front | Back |
What is another word for "necrosis"?
|
Oncotic cell death/oncosis
|
Histologic changes seen in necrosis
|
Membrane whorls and other myelin
figures, mineralization, eosinophilia
|
Why is eosinophilia seen in necrosis?
|
Loss of ribosomes and denaturation of proteins
|
Signs of necrosis on electron microscopy
|
Surface blebbing, detachment of actin filaments from plasma membrane, mitochondrial swelling, mineralization, ER and golgi fragmentation
|
When do you know that you have passed the "point of no return"? What is the "final blow" leading to this point?
|
When the nucleus becomes pale and fades away - unregulated influx of Ca++
|
What is the specific name for the fading of the nucleus?
|
Karyolysis
|
What information is given by the dye exclusion test?
|
Differentiates between necrosis (cells will passively accumulate dye through pores in membrane) and apoptosis (cells do not accumulate dyte)
|
Does necrosis usually affect multiple or single cells? What about apoptosis?
|
Necrosis - multiple cells
Apoptosis - single cells
|
Is apoptosis energy-dependent or -independent?
|
Dependent
|
Does apoptosis involve inflammation?
|
No
|
Pathologic examples of apoptosis causes
|
CTL immune response, injury from toxins and drugs, irradiation injury, regression of hyperplasia or during tissue atrophy, malignant neoplasms
|
Main enzyme family responsible for apoptosis
|
Caspases
|
General mechanism of caspase action
|
Proscaspases (inactive form) are activated in a progressive cascade - eventually activate enzymes such as endonucleases
|
Caspase extrinsic pathways mainly involve _____ while intrinsic pathways involve ______
|
Cell surface receptors, mitochondria
|
What other non-caspase molecules are involved in apoptotic pathways? (2)
|
Endoplasmic reticulum and the regulatory molecule p53
|