Hyperplasia
Fat necrosis (saponification of fat derived from peripancreatic fat cells exposed to pancreatic enzymes is a feature typical of fat necrosis); saponification is NEFA’s binding with Ca to form soaps)
Glandular metaplasia (since you’re going from squamous epi to the simple columnar epi of the small intestine)
Metastatic calcification
Atrophy
Abnormal pattern of cell maturation (dysplasia of the bronchial epithelium and is a reaction of respiratory epi to carcinogens in tobacco smoke)
mRNA: hypertrophy results from transcriptional regulation!!
Dystrophic calcification (underlying cell injury; serum levels of calcium normal, and calcium deposits located in previously damaged tissue)
Plasma membrane sodium transport (hydropic swelling reflects acute, reversible cell injury; reflects impaired cellular volume regulation, a process that controls ionic concentrations in the cytoplasm)
Intermediate filaments (what makes up alcoholic hyaline)
Anthracosis: storage of carbon particles in lung and regional lymph nodes
We see hyperplasia (islet cells of pancreas with proliferative capacity and respond to increased demand for insulin)
Liquefactive necrosis: rate of dissolution of necrotic cells faster than rate of repair
Caseous necrosis
Pyknosis
Humoral and cellular immunity
Hypertrophy
Higher IC levels Ca
Atrophy
Coagulative, or ischemic necrosis (lack of O2 impairs mito electron transport, decreasing ATP synthesis
Nuclear fragmentation (hallmark of COAGULATIVE necrosis)
Advanced age (lipofucsin)
Peroxidation of membrane lipids (lipofuscin found in lysosomes and has peroxidation products of unsaturated FA’s
Hemosiderin (denatured form of ferritin that aggregates easily and is recognized microscopically as yellow-brown granules in cytoplasm and turn blue with Prussian blue)