Fou 6 - Cellular Suffering and Death Flashcards
(42 cards)
How many pathway are there for apoptosis ?
Two: Intrinsic and extrinsic.
Which is the final step for apoptosis?
Activation of cytosolic caspases that mediate cellular breakdown.
What histological findings characterize Apoptosis?
Deeply eosinophilic cytoplasm, cell shrinkage, Nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, Nuclear fragmentation (Karyorrhexis), and formation of apoptotic bodies.
What is Pyknosis?
Nuclear shrinkage
What is Karyorrhexis?
Nuclear fragmentation.
In the Intrinsic pathway, what happened with the proportion of the Anti- and Pro- apoptotic factors?
Changes in proportion more pro- than anti-.
Which are the Pro- and Anti- apoptotic factors?
Pro- BAX and BAK proteins.
Anti- Bcl-2
What is the BAX and BAK’ functions?
Increased mitochondrial permeability and Cytochrome C release.
What is the function of the Apaf-1?
Normally induces the activation of caspases.
Which is the process of the Follicular lymphoma?
Occurs when Bcl-2 is overexpressed, then decrease caspase activation and tumorigenesis.
Which is the function of the BCL-2?
It is the major anti-apoptotic regulator of the mitochondrial permeability.
What is the primary initiator of the apoptosis?
Caspases.
Which is the pathway characterized by death receptors?
Extrinsic pathway.
Which are the two death receptors?
Fas receptor activated by FasL (Fas ligand). TNF receptor activated by TNF-Alpha
What is the function of Granzyme B?
Activate caspases directly.
Which defective interaction of the apoptosis process contribute to autoimmune disorders?
Defective Fas-FasL interactions.
What is the protein that is use by Killer T cells to make holes in plasma membrane?
Perforin punches holes in membrane.
Definition of necrosis:
Enzymatic degradation and protein denaturation of cell due to exogenous injury produce intracellular components leak. Inflammatory process (unlike apoptosis).
What does apoptosis mean?
Programmed cell death or orderly cell death process.
How many types of necrosis are there?
Coagulative, Liquefactive, Caseous, Fat, Fibrinoid, Gangrenous.
What is Coagulative necrosis?
Seen in: ischemia/infarcts in most tissues(except brain). Due to: ischemia/infarction; proteins denature, enzymatic degradation.
Histology: Cell outlines preserved; increased cytoplasmic binding of acidophilic dyes.
What is Liquefactive necrosis.
Seen in: Bacterial abscesses, Brain infarcts (due too increase fat content).
Due to: Neutrophils releasing lysosomal enzymes that digest the tissue.
Histology: Early (cellular debris and macrophages) and Late (cystic spaces and cavitation brain).
What is Caseous Necrosis
Seen in: TB, systemic fungi (histoplasma capsulatum), Nochardia. Due to: Macrophages wall off the infecting microorganism, that produces granular debris. Histology: Fragmented cells and debris surrounded by lymphocytes and macrophages.
What is Fat Necrosis?
Seen in: Enzymatic (acute pancreatitis, saponification) and Nonenzymatic (Breast trauma). Due to: Damaged cells release lipase, which breaks down fatty acids in cell membranes. Histology: outlines of dead cells without peripheral nuclei;saponification of fat (with calcium) appears dark blue on H&E stain.
