Inflammation I Flashcards
(22 cards)
What is apoptosis?
Programmed cell death requiring ATP (p.212)
What are the two pathways of apoptosis?
Intrinsic and extrinsic- both involve activation of cytosolic caspases that mediate cellular breakdown (p.212)
How much inflammation is involved in apoptosis?
No significant inflammation (p.212)
What characterizes apoptosis?
Characterized by cell shrinkage, nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, nuclear fragmentation (karyorrhexis), and formation of apoptotic bodies which are subsequently phagocytosed (p.212)
What is karyorrhexis?
Nuclear fragmentation (p.212)
Name three instances where the intrinsic pathway of apoptosis used.
1.) Involved in tissue remodeling in embryogenesis; 2.) Occurs when a growth factor is withdrawn from a proliferating cell population (e.g. decreased IL-2 after a completed immune reaction causes apoptosis of proliferating effector cells); 3.) Occurs after exposure to injurious stimuli (radiation, toxins, hypoxia, etc.) (p.212)
What changes lead to increased mitochondria permeability and cytochrome c release in the intrinsic pathway of apoptosis?
Changes in the proportions of anti- and pro- apoptotic factors (p.212)
What are the two pathways associated with the extrinsic pathway of apoptosis?
1.) Ligand receptor interactions (Fas ligand binding to Fas CD95); 2.) Immune cell (cytotoxic T cell release of perforin and granzyme B) (p.212)
Define necrosis.
The enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components extravate. (p.212)
What is the principle difference between apoptosis and necrosis?
Necrosis is an inflammatory process; apoptosis is not (p.212)
Name the 6 types of necrosis.
1.) Coagulative; 2.) Liquefactive; 3.) Caseous; 4.) Fatty; 5.) Fibrinoid; 6.) Gangrenous (p.212)
Where does coagualtive necrosis occur?
Heart, liver, kidney (p.212)
Where does liquefactive necrosis occur?
Brain, bacterial abcesses, pleural effusions (p.212)
What are the two types of gangrenous necrosis?
Dry (ischemic coagulative) or wet (with bacteria) (p.212)
Where does caseous necrosis occur?
TB, systemic fungi (p.212)
Where does fatty necrosis occur?
Peripancreatic fat (p.212)
Where does fibrinoid necrosis occur?
Blood vessels (p.212)
Where does gangrenous necrosis occur?
Limbs and in the GI tract (p.212)
What are the six hallmark signs that cell injury is reversible with oxygen?
1.) decreased ATP synthesis; 2.) cellular swelling (no ATP causes impaired Na/K pump); 3.) Nuclear chromatin clumping; 4.) decreased glycogen; 5.) fatty change; 6.) ribosomal detachment (decreased protein synthesis) (p.213)
What are the five hallmark signs that cell injury is irreversible?
1.) Nuclear pyknosis, karyolysis, karyorrhexis; 2.) Calcium influx –> caspase activation; 3.) Plasma membrane damage; 4.) Lysosomal rupture; 5.) Mitochondrial permeability (p.213)
What areas of the brain are most susceptible to hypoxia and ischemia/ infarction?
ACA/MCA/PCA boundary areas (p.213)
What areas of the heart are most susceptible to hypoxia and ischemia/ infarction?
Subendocardium (LV) (p.213)
