Cells and Genetics Flashcards
Cellular injury
Result of a stimulus in excess of the cells adaptive response
Cellular adaptation
Compensation that occurs at the cellular level
Where will hyperplasia not take place?
Cells that can’t replicate (heart, neurons, muscle, etc)
Dysplasia
cells that are abnormal in size, shape, or organization. These are abnormal cells that are not necessarily cancer. Ex- wart
Cancers will be
dysplastic and neoplastic
Neoplasia
Abnormal, disorganized growth (a tumor). May or may not be cancer.
4 Themes of cellular injury
1) ATP depletion (often due to lack of O2)
2) Free radicals and reactive oxygen species (cause oxidation of membranes and other structures, often a problem with re-perfusion)
3) Increase in intracellular Ca++ (release of Ca from mitochondria, lack of ATP to remove it, activation of many enzymes from Ca, very high Ca levels signal apoptosis)
4) Defects in plasma membrane (loss of normal cell function, loss of Na+ gradient, activation of proteases and phospholpases)
Marker of cellular death
Creatine kinase
Result of intracellular decrease in pH
Nuclear chromatin clumping and swelling of lysosomes (this welling then causes a release of lysosomal enzymes that begin autodigestion)
2 key players in irreversible cell injury
Lack of ATP generation and major damage to membrane function
Most common cause of cellular injury
Hypoxia
Most common cause of hypoxia
Ischemia
Ischemia
Inefficient blood supply to tissue or ogan
Infarction
Ischemia with necrosis
How does a reperfusion injury occur?
Reperfusion with oxygen results in the production of xanthin oxidase, which goes on to make massive amounts of superoxide, H2O2, and nitric oxide (another free radical). Basically, the reperfusion results in formation of ROS that can cause necrosis.
Main oxidants in our bodies
Superoxide anion, hydrogen peroxide, and hydroxyl radical. We want to get rid of these ASAP!!
O2- is converted to _____ by ______
O2 and H2O2 Superoxide dismutase (SOD)
Hydroxyl radical is converted to ______ by _____
H2O2
Glutathione peroxidase
H2O2 is converted to _______ by _____
H2O
Catalase
Interestingly, animals with more catalase tend to live longer
How is O2 converted into O2- (superoxide)?
By oxidative enzymes in the mitochondria, ER, plasma membrane, peroxisomes, and cytosol.
Process of apoptosis
Initial changes include nuclear chromatin condensation and fragmentation, followed by cellular shrinking & budding, and phagocytosis of those apoptotic bodies. No cytoplasm is released during apoptosis and it does not result in an inflammatory response!
Process of coagulation necrosis
Chromatin clumping, organelle swelling, and eventual membrane damage. Cytoplasm will leak and release intracellular enzymes. Immune system is recruited.
Point to note between necrosis and apoptosis
Apoptosis involves cellular shrinking and then budding. Necrosis involves swelling and lysis.
4 Types of Necrosis
Coagulative
Liquefactive
Caseous
Fat
Coagulative necrosis
Usually due to ischemic infarction anywhere except the brain. In this type of necrosis, everything is dead, but the cytoskeleton and general cellular structure remain intact
Liquefactive Necrosis
This involves enzymatic digestion of cells to form a liquid, viscous mass. Usually due to a bacterial or fungal infection d/t it’s ability to stimulate an inflammatory response. After removal of cellular debris by WBCs, a liquid filled space is left. This type of necrosis occurs in the brain because it has many digestive enzymes and little connective tissue. The cell architecture is lost in this type of necrosis, which is why it is liquid. Pus is also liquefactive necrosis.
Caseous necrosis
Happens as a result of TB infections. Looks like a yellow-white, cheesy debris. This is kind of like a combo between coagulative and liquefactive necrosis.
Fat necrosis
In this necrosis, lipases act on fats. This results in the release of ffas from triglycerides. These ffas then complex with calcium to form soaps, which appear as white, chalky deposits. This is often associated with pancreatitis. This is also why those with pancreatitis have low Ca levels.
Dry gangrene
A form of coagulative necrosis and is due to ischemia (lack of arterial blood flow).
Wet gangrene
This is coagulative necrosis progressing to liquefactive necrosis, and usually happens in parts of the body that are naturally moist. This is often characterized by thriving bacteria and has poor prognosis due to septicemia. As opposed to dry gangrene, this is often due to blockage of venous flow (the affected part is saturated with stagnant blood)
These cells have active telomerase activity
Germ cells and stem cells. However, only germ cells have sufficient levels of telomerase to maintain telomere length indefinitely.
Number of replications we have per telomere
40-60
BUN and creatinine are monitors of kidney function, but they can be influenced by
BUN- also reflects diet and hydration
Creatinine- can go up and down with how much muscle mass you have