Quiz 1 Review More Cowbell
Quiz 1 review Inflamma7on Repair Cell Injury and Adapta7on
Quiz 1 review Inflamma7on
Injury Acute inflammation Chronic inflammation Abscess Resolution Repair
Time course Inflammation Acute inflammation: Less than 48 hours Chronic inflammation: Greater than 48 hours (weeks, months, years) Cell type Acute inflammation: Polymorphonuclear leukocyte (PMN) Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells)
Injury Acute inflammation Chronic inflammation Abscess Resolution Repair
Changes in vascular flow and caliber (hemodynamic changes) Vasoconstriction Vasodilatation Slowing of the circulation Leukocyte margination
Leukocyte exudation divided into 4 steps 1. Margination, rolling, and adhesion 2. Diapedesis (transmigration across the endothelium) 3. Migration toward a chemotactic stimulus 4. Phagocytosis
Acute meningi7s: pus overlying brain surface
Bacterial meningi7s: neutrophils in subarachnoid space
Same case, higher power: mostly neutrophils
Injury Acute inflammation Chronic inflammation Abscess Resolution Repair
Chronic Inflammation Time course: Greater than 48 hours (weeks, months, years) Cell type Mononuclear cells (Primarily Macrophages, Lymphocytes, Plasma cells)
Acute viral meningi7s: lymphocytes in subarachnoid space
Granuloma with mul7nucleated giant cells and lymphocytes
Quiz 1 review Inflamma7on Repair
Tissue Repair Tissue repair = restora7on of 7ssue architecture and func7on aher an injury Occurs in two ways: Regenera7on of injured 7ssue Replacement by connec7ve 7ssue (scarring) Usually, 7ssue repair involves both processes Involves cell prolifera7on, and interac7on between cells and extracellular matrix
Cellular Prolifera7on Tissues of the body are divided into three groups: Con7nuously dividing (labile) 7ssues Easily regenerate Bone marrow, epithelia Stable 7ssues Can regenerate (but limited) Liver, kidney, pancreas Permanent 7ssues Can t proliferate Heart, neurons
The Cell Cycle and Different Cell Populations
Granula7on 7ssue
first intention healing second intention healing
Quiz 1 review Inflamma7on Repair Cell injury and adapta7on
! Normal cells have a fairly narrow range of function or steady state: Homeostasis! Excess physiologic or pathologic stress may force the cell to a new steady state: Adaptation! Too much stress exceeds the cell s adaptive capacity: Injury
! Cell injury can be reversible or irreversible! Reversibility depends on the type, severity and duration of injury! Cell death is the result of irreversible injury
Summary: Dr. Dolan slides 4-25 Cell injury starts with mitochondrial injury. ATP means pumps don't work well. Sodium and calcium accumulate inside cell. Free radicals damage cell membrane. The ul7mate reasons the cell dies are: membrane damage and cytoplasmic calcium accumula7on.
Summary: Dr. Dolan slides 4-25 Things you see in reversible injury: Mitochondrial densi7es Cellular swelling Cytoskeletal disrup7on (microvilli loss, blebs) Things you see in irreversible injury: All of the reversible changes, plus: Increased eosinophilia (pink color) in cells Bigger mitochondrial densi7es Nuclear changes (pyknosis, karyolysis, karyorrhexis)
! Pyknosis! Nuclear shrinkage and increased basophilia! Karyorrhexis! Fragmentation of the pyknotic nucleus! Karyolysis! Fading of basophilia of chromatin
! Apoptosis! Usually a regulated, controlled process! Plays a role in embryogenesis! Necrosis! Always pathologic the result of irreversible injury! Numerous causes
! Coagulative (most common)! Liquefactive! Caseous! Fat necrosis! Gangrenous necrosis
Summary: Types of Necrosis Coagula7ve Ghostly cell outlines, nuclear changes (like pyknosis) Seen in infarc7on (dead 7ssue from lack of blood supply Liquefac7ve Tissue dissolves (liquid!) Seen in abscesses and in CNS injuries Caseous Cheesy grossly, amorphous debris and inflamma7on Seen in tuberculosis Fat necrosis Dissolved fat reacts with calcium = chalky deposits Seen with trauma to fady organs (pancreas, breast) Gangrenous necrosis Large areas of dead 7ssue due to lack of blood supply Seen usually in extremi7es
! Increase in the number of cells in an organ or tissue! May or may not be seen together with hypertrophy! Can be either physiologic or pathologic
! Shrinkage in the size of the cell (with or without accompanying shrinkage of the organ or tissue)! Atrophied cells are smaller than normal but they are still viable they do not necessarily undergo apoptosis or necrosis! Can be either physiologic or pathologic
! A reversible change in which one mature/ adult cell type (epithelial or mesenchymal) is replaced by another mature cell type! If injury or stress abates, the metaplastic tissue may revert to its original type! A protective mechanism rather than a premalignant change