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
systemic change of necrosis - trophic response
general decrease in blood supply to a body part
scaly, cold, shiny, alopecia, puffy, dec pedal pulse
Fibrinoid necrosis
- occurs on the endothelial lining of blood vessels and is caused by an accumulation of proteins in the plasma and cellular debris
- form “sludge” deposits on vessel
**caused by: autoimmune vasculitis or organ transplant rejection
Coagulative necrosis
- small area of general ischemia
- tissue firm and red, resembles egg white after boiling
- protein becomes denatured
ex) cystic acne
Liquefactive/ Colliquative necrosis
lysosomes liberate enzymes; results in tissue breakdown and liquefaction
Caseation necrosis
type of tissue destruction that is only partial and complete
“cheesy” appearance
caused by TB
“keep cheese in the cold CASE”
Fatty necrosis
normal functioning tissue that is replaced by fat
gives the tissue a “chalk” appearance
Pathologic tissue (dystrophic) calcification
necrotic tissue binds calcium from the body fluids to form histoliths (stones embedded in tissues); hardening
common example of pathologic tissue
myositis ossifications
may occur in injury to the thigh muscles or tuberculosis or atherosclerosis
cellular senescence
aging of cells
lack of apoptosis can cause
syndactyly (webbed)
age related DNA copy mutations
As these cells divide over and over, there can be DNA mutations that can cause diseases
aging in CNS
senile atrophy: losing brain tissue, starts in hippocampus
Lewy Bodies
proteins produced by neurons
- begin producing alpha-synuclein aggregate that causes dementia (hallucinate); can only diagnose w/ autopsy
parkinson’s?
Genetic pre-mature aging (Progeria)
rapidly aging system because of a cell mutation
signs of aging
Loss of skin elasticity
Decline in resistance to infections
Atherosclerosis—lipid plaques
DNA Mutation—Neoplasia
mechanisms and manifestations of cellular injury
Infectious agents Immune reactions Genetic factors Nutritional factors Physical factors Chemical factors
Often injuries are reversible and sub-lethal so cells can repair themselves through regeneration
If severe enough and of great magnitude, then cells may die and repair has to occur via replacement with nonfunctional or scar tissue
