Quiz 1 Review. More Cowbell

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1 Quiz 1 Review More Cowbell

2 Quiz 1 review Inflamma7on Repair Cell Injury and Adapta7on

3 Quiz 1 review Inflamma7on

4 Injury Acute inflammation Chronic inflammation Abscess Resolution Repair

5 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)

6 Injury Acute inflammation Chronic inflammation Abscess Resolution Repair

7 Changes in vascular flow and caliber (hemodynamic changes) Vasoconstriction Vasodilatation Slowing of the circulation Leukocyte margination

8 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

9 Acute meningi7s: pus overlying brain surface

10 Bacterial meningi7s: neutrophils in subarachnoid space

11 Same case, higher power: mostly neutrophils

12 Injury Acute inflammation Chronic inflammation Abscess Resolution Repair

13 Chronic Inflammation Time course: Greater than 48 hours (weeks, months, years) Cell type Mononuclear cells (Primarily Macrophages, Lymphocytes, Plasma cells)

14 Acute viral meningi7s: lymphocytes in subarachnoid space

15 Granuloma with mul7nucleated giant cells and lymphocytes

16 Quiz 1 review Inflamma7on Repair

17 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

18 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

19 The Cell Cycle and Different Cell Populations

20 Granula7on 7ssue

21 first intention healing second intention healing

22 Quiz 1 review Inflamma7on Repair Cell injury and adapta7on

23 ! 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

24 ! 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

25 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.

26 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)

27 ! Pyknosis! Nuclear shrinkage and increased basophilia! Karyorrhexis! Fragmentation of the pyknotic nucleus! Karyolysis! Fading of basophilia of chromatin

28 ! Apoptosis! Usually a regulated, controlled process! Plays a role in embryogenesis! Necrosis! Always pathologic the result of irreversible injury! Numerous causes

29 ! Coagulative (most common)! Liquefactive! Caseous! Fat necrosis! Gangrenous necrosis

30 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

31 ! 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

32 ! 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

33 ! 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

PREPARED BY P.DHARANI PRASAD II YEAR B.PHARM II SEM SUB:PATHOPHYSIOLOGY

CELL INJURY UNIT I PREPARED BY P.DHARANI PRASAD II YEAR B.PHARM II SEM SUB:PATHOPHYSIOLOGY DETECTION OF CELLULAR CHANGES AFTER INJURY BY: LIGHT MICROSCOPY OR GROSS EXAMINATION DETECT CHANGES HOURS TO DAYS