Cell Injury Flashcards
Cell adapation
Process by which cells change in size, number, and appearance in response to changes in cell environment
Hyperplasia
Increase in number of cells
Physiologic: glandular epithelium of the breast during pregnancy
Pathologic: abnormally high levels of estrogen can cause proliferation of endometrial gland epithelium (endometrial hyperplasia)
Hypertrophy
Increase in the size of a cell because of increased cellular substance
Physiologic: skeletal muscle in an athlete who repeatedly lifts weights
Pathologic: patient with systemic hypertension will increase cardiac muscle mass because heart must work harder to overcome vascular resistance
Atrophy
Decrease in size of a cell because of loss of cellular substance
Physiologic: what happens to the endometrium of a post-menopausal woman
Pathologic: muscles will atrophy when leg is placed in a cast for a broken bone
Metaplasia
Substitution of one type of adult cell for another type of adult cell
Clinical example: normal endocervix and endocervical glands are lined by simple columnar epithelium
Chronic irritation and inflammation of the cervix uteri may cause replacement of columnar cells by stratified squamous cells
Hypoxic Injury Model
Ischemia, hypoxemia, decreased O2 carrying capacity
Loss of energy, increased in cellular calcium which leads to altered membrane permeability and activation of intracellular enzymes
Intracellular enzymes leak from cell into vascular compartment, can be measured clinically (elevated CK or troponin in MI, or AST/ALT in hepatitis)
Cell switches from aerobic to anaerobic respiration, lactic acid levels are increased and can be measured (lactate clearance is an emerging way of confirming adequate resuscitation in shock)
Free Radical Injury Model
Chemically unstable and very reactive with components of the cell
Carbon tetrachloride (CCL4) is converted to CCL3 by hepatocytes which causes lipid peroxidation and damage to cell structures
Reperfusion injury: Return of blood./oxygen to ischemic tissue, free radicals are produced, which paradoxically causes further damage to cells
Reversible cell injury
Cellular swelling Steatosis Myelin figures ER swelling Membrane blebs
Irreversible cell injury
Pyknosis ( irreversible condensation of chromatin), loss of nuclei, fragmentation of cells, leakage of contents
Necrosis
Characterized by the presence of leukocytes (especially neutrophils), morphologic changes occur as result of enzymatic breakdown of cell and denaturation of proteins
Coagulation necrosis
From severe ischemia In solid organs (heart, kidney) Microscopic: ghost-like remnants of intact cells which lack nuclei, cell outline is preserved and cytoplasm stains intense pink (eosinophilia) Macroscopic: tissue firm Ex: myocardial infarct, renal infarct
Liquefactive necrosis
Associated with bacterial infections
Microscopic: bacteria release enzymes causing a rapid loss of cellular structure and a collection of liquid, amorphous debris
macroscopic: creamy yellow material
-abscess: collection of neutrophils, dead cells, liquid
Ex: brain hypoxia/infarct
Caseous necrosis
Pattern of necrosis associated with an inflammatory reaction called “granuloma”
Histologically: amorphous, granular debris (dead cells) in the center of granulomatous cell reaction
macroscopically: necrotic tissue is soft, white, friable
“cheese curd”
Enzymatic fat necrosis
Focal cell death in the pancreas and adjacent fat
Ex. acute pancreatitis
White chalky deposits represent calcium soap formation at sites of lipid breakdown
Gangrene
Clinical term
Represents coagulation (ischemic) necrosis, usually of an extremity, bowel, gallbladder
If bacteria contaminate dying tissue, superimposing liquefactive necrosis, the process is referred to as wet gangrene
