Parsa- Cell injury 3 and 4 Flashcards
how does ATP become depleted?
stop oxygen supply or nutrient supply in an artery, toxins (cyanides). without oxygen than the mitochondria wont be able to do oxidative phosphorylation.
if a patient is experiencing anaerobic ATP production due to lack of oxygen, what would you notice in the cell?
clumping of nuclear chromatin due to a decrease in pH
if there is an influx of calcium, water, sodium and an efflux of potassium; what is not working correctly? and how will it effect the cell?
sodium pump is faulty.
leads to ER swelling, cellular swelling, blebs and loss of microvilli
if cytochrome c is released from the mitochondria what will happen?
apoptosis
how does loss of membrane potential lead to necrosis?
decrease oxidative phosphorylation-> inability to make ATP
what can independently activate caspases to undergo apoptosis?
calcium
how does oxidative stress occur in a cell?
when the production of ROS increases or the scavenging systems are ineffective.
what mechanisms in the cell help to reduce the amount of ROS in the cell?
antioxidant mechanisms (Superoxide dismutase, glutathione peroxidase, catalase)
what generally accompanies ischemic injury?
inflammation because neutrophils and other leukocytes are usually present
how does inflammation further antagonize ischemic injuries?
Reperfusion. (inflammation also leads to ROS byproducts. so ROS increases due to inflammation and ischemia)
what is considered to be a sign of cell death?
leakage of enzymes
ischemic attacks like sickle cell disease tend to disrupt blood supplies. if an organ like a liver exhibit a firm texture in which the architecture of dead tissues is preserved for a span of a few days, what type of necrosis is it?
coagulative necrosis
what type of tissues tend to experience hemorrhagic necrosis?
in tissues when venous supply is obstructed and leads to rupture. (common in the lungs and reproductive system)
what is the difference between coagulative necrosis and liquefactive necrosis?
in contrast to coagulative necrosis, it is characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass (ischemic attack in the brain).
what kind of necrosis is exemplified by blockage of arteries in the lower extremities in diabetic patients?
gangrenous necrosis
what kind of necrosis to patients with TB experience?
caseous necrosis (collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border).
what is similar to caseous necrosis, but also contains a lot of plasma cells?
gumma (common in syphilis)
what happens to a fat cell during fat necrosis?
irregular large bubble cell with no nucleus
what necrosis is usually deposited in the vascular walls due to the deposition of antigens and antibodies?
fibrinoid necrosis
what type of cells most commonly experience direct chemical injury (mercury binding to cell membrane sulfhydryl groups)?
absorption/ excretion cells (G.I and kidney)
when a person takes tylenol (acetaminophen) how much of it is converted to cytochrome P-450? and how is it detoxified?
5%
the free radical interacts with reduced glutathione (GSH) to become detoxified
are Bax and Bak considered anti-apoptotic?
nope. Bcl-2 and Bcl-x are anti-apoptotic
FADD is known to be the death signal domain in the extrinsic pathway. what activates the FADD?
when FasL bind to Fas
what can inhibit the pro-caspases-8 in the extrinsic pathway and ultimately inhibit apoptosis after FADD domain is active?
FLIP
what are the responses to misfolded proteins?
repair (chaperones), decreased translation of proteins, activation of ubiquitin pathway (degradation) and activation of caspases (apoptosis)
