1st lecture (cell death) Flashcards
define death?
when the living bodies coordinated function is suspended and is irreversible; breathing, circulation, brain function is irreversibly stopped.
define Clinical death?
when the breathing, circulation and brain function is reversibly and temporary suspended.
Brain death definition?
when the function of the brain is irreversibly suspended.
2 types of postmortal changes?
early postmortal changes
late postmortal changes
Early postmortal changes?
- Palor mortis: paling of the body. (sedimentation of blood do the gravity)
- algor mortis: chilling of the body/or heating depending on the environmental temperature. 7-8 hours
- Rigor mortis: rigidity of the body do the muscles. Deficit of ATP causes rigidity. 2-4 hours later the body relaxes due to loss of muscle structure
- livor mortis: HYPOSTATIC: sedimentation of blood (opposite of palor mortis) do to gravity. INHIBITION: (happens later) the hemolysis of the RBC causes liberated Hb penetrating the surrounding tissue causing a pink-blue coloration around vessels, if you press on it, it will dissapear.
- Crusta mortis: coagulation of blood occurs hours after death (4 hours later) POST-mortal clot.
Nysten law?
muscle relaxation after death does not start in all the bodies muscle simultaneously. Starts in the face, and continues to the legs. (can be used to determine the time of death.)
compare the post-mortal-clot (PMC) with a thrombus?
SURFACE: PMC=shiny Thrombus=opaque
CONSISTENCY: PMC=rubbery Thrombus: Fragile
RELATION to vessels: PMC=slips easily out of vessels/no adhesion. Thrombus=will stick to the wall of vessels.
LATE postmortal changes?
- Exicatio postmortalis: loss of water; drying/shrinking
- Maceiatio: desqumation of cells from fluid containing structures like the bladder.
- gastromalacia: stomach and GI digests itself.
- Pseudomelanosis: blue discoloration
- Mumification: lack of fermintation of the bacteria means that there is a lack of bacteria destruction of the body
- adipocera: typical for bodies floating in water.
Pseudomelanosis definition?
GI flora bacteria make SH2 which reacts with hemoglobin making sulfur-hemoglobin with a blue color, resulting a blue discoloration around the large intestine.
adipocera definition?
characteristic of bodies who drowned in water and their bodies were floating in water for an extended period of time. their fatty acids bind the Na and K of the water making a waxy cover of the body.
after death there is a loss of water, what is this called?
Exicatio postmortalis
after death there is a desqumation of cells lining the structures such as the bladder, what is this called?
maceiatio
what is it called when the GI tract digests itself after death?
gastromalacia
Define necrosis?
dissociation of cell, autolysis, heterolysis (another cell digests its)
dead cells/tissues/organs in a living body. the cells digestive enzymes are activated and released digesting itself as mitochondria and golgi membranes break down releasing enzymes.
inflammatory cells: macrophages and polymorphonuclei go to the area and release digestive enzymes, and phagocytose the necrotic cell.
causes of necrosis?
- Oxygen deprivation, hypoxia: drop in oxygen levels in the blood or anemia. Ischemia occlusion of the vessel.
- Chemicals; acids, alkaline
- inflammation; immune competent cells kill injured cells.
- nutritional imbalance: too much, too little nutrition.
- physical agents: chemical, heat, radiation.
Morphology; how to recognize a necrotic cell.
acidophillic/eosinophilic cytoplasm due to:
- pH dropping
- decrease in protein synthesis which is normally basophilic (lack of blue)
- vacules in cytoplasm; dilated golgi and ribosomes and mitochondria, which are dilated due to lack of energy to keep their shape. (myelin figure, membrane disintegrated, the fatty acids uptake water.)
- Nuclear fragmentation: (karyorrhexis)
- chondensation of chromatin (picnosis)
- kardiolysis: shadow of former nucleus (karyolysis)
define karyorrhexis:
fragmentation of the nucleus of the cell
fate of necrotic cells?
- could stay here
- generate a inflammatory response
- regeneration of new cell in the area
calcification of necrotic cells?
necrotic cells can pick up calcium.
events of necrosis? (in order that they occur)
- hypoxia/ischemia (which then causes:)
- Ca2+ influx (which then causes:)
- Reperfusion injury (which then causes:)
- ER stress
- toxins can also play a role
during Necrosis the hypoxia/ischemia causes what?
DECREASE of oxidative phosphorylation causes ATP drop. The affected Na+ pump shuts down and water influx causes swelling.
ANAEROBIC GLYCOLYSIS = drop in glycogen = Ph drop
DETACHMENT of ribosomes, DROP in protein synthesis as structural elements of cells are lost.
during Necrosis the Ca2+ influx
there is a 10,000x difference between intracellular and extracellular Ca concentration. the ATP dependent Ca2+ pump shuts down. Ca2+ influx from mitochondria and SER. the high Ca2+ activates enzymes; protease, lipases, DNase.
THIS IS THE POINT OF NO RETURN.
During necrosis describe Reprefusion injury?
O2 levels are low —-> Cells make ROS —-> H2O2, O-. (these are normally neutralized by mitochondria enzymes, but lack of blood flow kills the mitochondria 1st) —-> ROS cause;
Lipid peroxidation, DNA fragmentation, protein crosslinking.
since the mitochondria is already destroyed reperfusion causes and increase in oxygen supply, resulting in more ROS do to the lack of enzymes to neutralize them.
— polymorphic cells may detect damaged cells and release ROS to kill the cell and activate complement system.
during necrosis what is Endoplasmic reticulum stress?
The ER produced protein which have to be properly folded by chaperons. Chaperons may be suspended due ER stress resulting in misfolded proteins accumulation.
