Apoptosis and necrosis Flashcards
Programmed destruction of cells during embryogenesis
Apoptosis
Hormone dependent involution
Apoptosis
In endometrium during menstrual cycle
Hormone dependent involution
Physiological
Apoptosis
Prostate atrophy after castration
Pathological hormone dependent involution
Apoptosis
Cell deletion in proliferating tissues e.g. cell death in tumors
Apoptosis
deletion of autoreactive T-lymphocytes in thymus
Immune cell death apoptosis
cell death induced by cytotoxic T cells
Immune cell death apoptosis
mild heat, radiation, cytotoxic treatment.
Mild injurious stimuli apoptosis
Alzheimer disease
Death of neurons in disease processes ,apoptosis
Enzymes which are present in the cytoplasm and are key players in apoptosis
Found in an inactive form in the cytoplasm.
Caspases
Caspases name meaning
They are called Caspases from C; from Cysteine active site, “asp”; from cleavage after aspartic acid residue.
signaling of these caspases results in commitment of cells to apoptotic cell death. These are found in certain cell types.
Initiators
these are proteases which bring about the structural degradation of the cells to give the classical morphology. They are present in all cell types.
Effectors
BCL-2 / BCL-XL
suppress apoptosis
Bax / Bad
Enhance apoptosis
protects from apoptosis by stabilizing the mitochondrial membrane, thus preventing increase permeability, by binding and sequestering cytochrome-C, and stabilizing proteins like the Apaf, thus preventing its activation.
Bcl-2
Mitochondrial damage mechanism of apoptosis
Stimuli like toxins, or signalling will open permeability transition pore complex (PTPC), or mega channels, which will release material mainly cytochrome-C from the mitochondria to cytosol.
Cytochrome-C will bind to Apaf “pro-apoptotic protease-activating factor” and activate effector caspases
intrinsic or extrinsic triggers to induce apoptosis like low ATP and high ROS
Signaling
Apoptosis execution
by caspases that activate cytoplasmic endonuclease and proteases that degrade cytoskeletal & nuclear proteins which results in breakdown of cytoskeleton and fragmentation of nuclear chromatin.
Apoptosis Control and integration
by the BCL-2 family that can either inhibit or promote cell death.
Removal of dead cells
the formation of apoptotic bodies containing various intracellular organelles; they express new ligands that mediate phagocytic cell binding and uptake
Apoptosis morphology
Single cells or groups of cells
Cells show intensely eosinophilic cytoplasm and condensed pyknotic nucleus
Cells are not surrounded by inflammatory cells
Rapidly removed by fragmentation and engulfment by cells
Pyknosis
increased basophilia due to shrinkage of the nucleus
chromatin clumping organellar swelling membrane damage Enzymatic digestion and leakage of cellular contents
Necrosis
chromatin condensation chromatin fragmentation cytoplasmic budding
Apoptosis
Intact membrane ; altered structure, especially orientation of lipids
What type of death?
Apoptosis
Cellular contents Intact; may be released in apoptotic bodies
Apoptosis
may be pathologic after some forms of cell injury, especially DNA damage
Apoptosis
Apoptosis nuclear change
Fragmentation into nucleosome size fragments
death of cells with preservation of the basic structural outlines of the cells for days
Protein denaturation overcomes enzymatic digestion
Seen in most organs after hypoxia/ischemia except brain
Coagulative necrosis
necrosis with complete digestion of the cells and destruction of the normal architecture
Enzymatic digestion overcomes the denaturation
Liquefactive necrosis
hypoxic/ischemic injury of the brain
What necrosis is it?
Liquefactive necrosis
bacterial/fungal infection, with accumulation of WBCs and release of enzymes
Liquefactive necrosis
cyst formation at the site of previous necrosis due
brain injury due to hemorrhage
Liquefactive necrosis
Special type of necrosis, seen with tuberculous infection
the tissue architecture is completely obliterated
Grossly:
cheesy white appearance to the necrotic focus Microscopically:
the necrotic focus is composed of structure-less amorphous granular debris
Caseous necrosis
Special type of necrosis with focal areas of fat destruction
Seen with acute pancreatitis, due to release of enzymes from the injured pancreas
Grossly:
fat saponification: visible white chalky areas
Microscopically:
shadows of cells with calcification
Fatty necrosis
Gangrenous necrosis
ischemic coagulative necrosis (Dry gangrene: frequently of a limb)
When there is superimposed infection with a liquefactive component, the lesion is called “wet gangrene”
