Unit I - Tissue and Necrosis Flashcards
pathophysiology
altered function resulting in disease, injury, or death
apoptosis
natural/programmed cell death
blebbing
changes to the cell membrane such as loss of membrane asymmetry and attachment, shrinkage, fragmentation
necrosis
traumatic cell death that results from irreversible cellular injury - so badly damaged that it’s going to die
lipofuscin deposits
pigment that develops in aging cells (brown spots on skin) from precipitation of unsaturated fats - if not metabolized properly it deposits in different parts of the body (eye)
encroach on the cell nucleus and affect wound healing
Beta-Amyloid protein
- form plaque in the CNS that kills neurons
* **main component of certain deposits found in brains of patients with Alzheimer’s
Tau protein
stabilize axonal microtubules
(found only in neurons) - they would be tangled without it, so this unfolds them and they are no longer protected
*also a cause of Alzheimer’s
free radicals
oxygen molecules that have given up a pair of electrons
borrow electrons from other tissues, which damages the tissues - contributes to aging/DNA mutations
Telomere aging clock theory
- after dividing so many times, the ends of chromosomes become damaged
free radicals try to replace lost electrons, so they borrow from other tissue molecules, resulting in DNA and tissue damage, accelerating the aging process
other factors that contribute to cellular aging
sedentary life style, obesity increased fat cells, type 2 diabetes, hypertension, decreased cardiac performance
2 outcomes to cell injurious event
reversible (sub-lethal)
irreversible (lethal) - necrosis
hydronic change (cloudy swelling)
reversible
accumulation of fluid inside the cell due to failure of the NA+K+ pump
intracellular accumulations (fatty change)
reversible
common in liver disease
hepatocytes become infiltrated with fat and form fatty inclusion bodies
cirrhosis/ Fatty liver disease
reversible
liver degeneration
associated with chronic alcohol abuse and/or hepatitis
microscopic changes in necrosis
nucleus fragmentation cytoplasm stains red mitochondria enlarged cell membrane becomes irregular cellular edema, lysosomes release enzymes that dissolve cells that causes inflammation, NA/K pump fails