Week 6 Tissue Injury- Nelson Flashcards
Hypertrophy
increased SIZE of cell leads to increase in size of organ or tissue
Results from increased production of cellular proteins
increased demand or stimulation
Ex: Thickness of left ventricle, uterus after pregnancy
Hyperplasia
increased NUMBER of cells leads to increase in organ or tissue
occurs if the cells of the organ can divide
increased demand or stimulation
Atrophy
decreased nutrients and decreased stimulation
Decrease in cell SIZE and NUMBER resulting in reduced size of tissue or organ
Common causes: Decreased workload loss of innervation diminished blood supply inadequate nutrition loss of endocrine stimulation pressure
Metaplasia
chronic irritation
adaptive response in which one differentiated type of cell is replaced by another cell type
Reprogramming of stem cells in normal tissue OR reprogramming of undifferentiated mesechymal cells
External stimuli
Ex: normal columnar epithelium changed to squamous metaplasia in lungs (loosing cilia) in smokers
Necrosis
loss of membrane integrity
Microscopic changes:
nucleus fades away, shrinks, cell content leaked out
specific proteins and enzymes can be detected in blood as diagnostic test
Apoptosis
Characterized by induction of REGULATED enzymatic suicide program that active intrinsic enzyme to degrade cells own DNA and nuclear/ cytoplasmic proteins
Causes:
DNA damage
accumulation of misfolded proteins
viral infection
Coagulative necrosis
architecture of dead tissue is preserved (infarct)
Liquefactive necrosis
digestion of the dead tissue results in liquid viscous mass, typically seen in focal bacteria or fungal infections. Lots of pus filled with neutrophils
Gangenous necrosis
clinical term, not specific. usually applied to necrosis of a limb undergoing coagulative ischemic necrosis
caseous necrosis
cheese-like necrosis associated with necrotizing granulomas
fat necrosis
focal areas of fat destruction
Fibrinoid necrosis
necrosis seen in immune reactions involving vessels
Describe mechanism of cell injury due to depletion of ATP
ATP is required for all synthetic degradative processes in the cell
caused by reduced blood supply of oxygen and nutrients, mito changes or exposure to certain toxins
Describe mechanism of cell injury due to mitochondrial damage
mito supply ATP to the cell through oxidative phosphorylation
damage caused by oxygen deprivation, oxygen free radials, increased cytosolic Ca+
results in defect in mito membrane, failure of ETC, depletion of ATP, formation of reactive oxygen species
escape of mitochondrial membrane proteins (cytochrome C)
Describe mechanism of cell injury due to influx of calcium and loss of calcium homeostasis
this may cause
mito membrane defect, no ATP generation, activation of lytic enzymes, induce apoptosis
Describe mechanism of cell injury due to oxygen derived free radials
Caused when production of ROS increases, scavenging systems are ineffective, or oxidative stress
may cause wide variety of conditions and diseases (chemical and radiation injury, ischemia reperfusion, cancer, aging, degenerative diseases
Mechanism of cell injury due to defects of membrane permeability
can occur due to ROS, decreased phospholipid synthesis (or increased breakdown), cytoskeleton abnormalities
Results in
mito membrane damage (decreased ATP)
Plasma membrane damage loss of osmotic balance, and cellular components,
release of lytic enzymes if lysosomal membranes compromised
When does injury become irreversible?
mitochondrial dysfunciton (depletion of ATP) and profound distrubance in membrane function (rupture of lysosomal and plasma membranes)
Define autophagy
a survival mechanism during nutrient deprivation can cannibalize itself and recycle the digested contents
What are the four main pathways of abnormal intracellular accumulations?
-abnormal metabolism (fatty change in liver associated with alcohol abuse) defect in protein folding/transport (excess cholesteral causing atherosclerotic vascular disease) lack of enzyme (glycogen storage diseases) ingestion of indigestible materials (Exogenous pigments like a tatoo)
Dystrophic calcifications
occurs in areas of necrosis
NORMAL serum calcium levels
Metastatic calcification
due to herpcalcemia secondary to disordered calcium metabolism
ELEVATED serum calcium levels
found in normal tissues
Cellular aging
result of progressive decline in cellular function and viability casued by genetic abnormalities and the accumulation of cellular and molecular damage due to effects of exposure to exogenous influences
Biochemical markers:
AST
found in liver, heart, skeletal muscle, brain and kidneys
Biochemical markers
ALT
liver
Biochemical markers
ALP
bile duct damage
Biochemical markers
Troponin 1
cardiac muscle