SECTION 2 CELL INJURY

Transcription

1 Adapted myocyte Normal myocyte Reversibly-injured myocyte SECTION 2 CELL INJURY Cell death 5/4/ /4/ Reversible Degeneration Irreversible Cellular Swelling Fatty Change Hyaline Change Amyloid Change Mucoid Change Pathologic Pigmentation Pathologic Calcification Cell Death Reversible Cell Injury Degeneration Intracellular &/or extracellular abnormal accumulation: Excess amounts of various normal substances (water,lipids,proteins,pigments) Abnormal substances (exogenous, endogenous) 5/4/ /4/ Cellular Swelling (1) Cellular Swelling (2) (hydropic degeneration) Intracellular accumulation Sodium Water Morphology the organs NE: Cloudy swelling Increase in the weight LM: EM: 5/4/ /4/

2 Cellular Swelling (3) Morphology Cellular swelling of liver NE: LM: the cells Large Small & fine granules in the cytoplasm Ballooning change EM: 5/4/ /4/ Cellular swelling in kidney cells 5/4/ Cellular swelling in liver cells 5/4/ Cellular Swelling (4) Morphology NE: LM: Swelling Endoplasmic reticulum EM: Mitochondria 5/4/ /4/

3 Mechanism Injurious agents Fatty Change (1) Mitochondria damage Steatosis ATP Water & sodium within the cells Cellular swelling Intracellular abnormal accumulation: Triglycerides Often occurred in the liver and the heart 5/4/ /4/ Fatty Change (2) Morphology Fatty Change (2) Morphology NE: LM: NE: LM: Large Yellow Soft Greasy EM: EM: 5/4/ /4/ Fatty Change (3) Morphology Fatty Change (4) Morphology NE: Fat vacuoles LM: Round, clear vacuoles Orange-red color by staining with Sudan Ⅲ or Oil Red O (Frozen tissue EM: sections!) NE: LM: EM: Liposomes Membrane-bound inclusions 5/4/ /4/

4 Fatty Change of the Liver (1) Fatty change in liver cells 5/4/ NE Mild fatty change: Not affect the gross appearance With progressive accumulation: Large Yellow Soft Greasy Fatty Liver: Severe & diffuse fatty change 5/4/ Fatty Change of the Liver (2) LM Fat vacuoles Small, in the cytoplasm around the nucleus Displacing the nucleus to the cell periphery Fatty liver 5/4/ Fatty cysts 5/4/ Fatty change of the liver 5/4/ Fatty change of the liver(sudan Ⅲ) 5/4/

5 Mechanism Fatty Change of the Liver (3) NE Fatty Change of the Myocardium Mild fatty change: Not affect the gross appearance With progressive accumulation: Tigered effect Apparent bands of yellowed myocardium alternating with bands of dark,red-brown,uninvolved myocardium 5/4/ /4/ Fatty change of heart muscle (tigered effect) 5/4/ Fatty change of heart muscle (tigered effect) Sudanhematoxylin 5/4/ Hyaline Change (1) A descriptive morphologic term Intracellular or extracellular abnormal accumulation: Proteins A homogeneous, translucent, pink appearance in HE staining 5/4/ /4/

6 Hyaline Change (2) Hyaline change in arteriolosclerosis e.g. Hypertension, Diabetes Hyaline change in connective tissues e.g. Old scars Hyaline change within the cytoplasm e.g. Nephrotic syndrome, Russell bodies, Mallory body 5/4/ Hyaline change in arteriolosclerosis 5/4/ Vascular pathology in hypertension. A, Hyaline arteriolosclerosis. The arteriolar wall is hyalinized, and the lumen is markedly narrowed. 5/4/ Chronic glomerulonephritis 5/4/ Protein reabsorption droplets in the renal tubular epithelium 5/4/ Mallory bodies in liver cells 5/4/

7 Amyloidosis Extracellular abnormal accumulation: Amyloid Hyaline Change 5/4/ /4/ Physicochemical characteristics of amyloid +Iodine--- a brown color--- +H 2 SO blue Staining: Congo red--- red, HE--- homogeneous pink EM: nonbranching fibrils nm wide X-ray: a pleated sheet structure (rendering protein very resistant to enzymatic degradation, contributing to its accumulation in tissues) This is a Congo red stain to reveal orange-red deposits of amyloid. 5/4/ /4/ Mucoid Change Extracellular abnormal accumulation: Mucopolysaccharide (Glycosaminoglycans, Hyaluronic Acid) 5/4/ /4/

8 Pathologic Pigmentation Intracellular & extracellular abnormal accumulation: Colored substances Exogenous Endogenous Pathologic Pigmentation Exogenous Carbon Endogenous Hemosiderin Lipofuscin Melanin 5/4/ /4/ Hemosiderin Carbon Hemosiderin granules in macrophages in the alveolus 5/4/ /4/ Lipofuscin Hemosiderin granules in liver cells. A, H&E B, Prussian blue reaction 5/4/ /4/

9 Pathologic Calcification (1) Melanin 1. Except for the bones and teeth 2. Pathologic conditions Intracellular & extracellular abnormal accumulation: Calcium salts 5/4/ /4/ This is dystrophic calcification in the wall of the stomach. 5/4/ /4/ Pathologic Calcification (2) Dystrophic Calcification In areas of necrosis No calcium metabolic derangements Metastatic calcification In normal tissues Some calcium metabolic derangements Adapted myocyte Normal myocyte Reversibly-injured myocyte Cell death 5/4/ /4/

10 Irreversible Cell Injury 1. Necrosis Cell Death A sequence of morphologic changes that follow cell death in living tissue 2. Apoptosis A distinctive and important mode of cell death regulated by genes Necrosis (1) Two essentially concurrent processes to produce the morphologic changes : 1. Enzymatic digestion of the cell Autolysis Heterolysis 2. Denaturation of proteins 5/4/ /4/ Necrosis (2) Basic pathologic changes Types of necrosis Sequences of necrosis Necrosis (3) Basic Pathologic Changes Pyknosis Nuclear changes Karyorrhexis Karyolysis Cytoplasm Increased eosinophilia 5/4/ /4/ Normal Pyknosis Necrosis (4) Types of Necrosis Karyorrhexis Karyolysis Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat necrosis Gangrene Fibrinoid necrosis Nuclear changes of necrosis 5/4/ /4/

11 Coagulative Necrosis A mass of coagulated, pink-staining, homogeneous cytoplasm Preservation of the basic structure outline of the coagulated cell or tissue for several days In solid organs (kidney, heart, spleen ) 5/4/ /4/ Liquefactive Necrosis Liquefaction of necrotic cells Condition: Presence of more abundant proteolytic enzymes Most often in suppurative inflammation & in the brain 5/4/ /4/ A small abscess in the liver Liquefactive necrosis of the brain (Encephalomalacia) 5/4/ /4/

12 Caseous Necrosis A distinctive form of coagulative necrosis Cheese-like An amorphous coarsely granular eosinophilic debris Most often in foci of TB 5/4/ A tuberculous lung with a large area of caseous necrosis. The caseous debris is yellow-white and cheesy. 5/4/ Fat Necrosis A special type of liquefactive necrosis Focal areas of fat destruction Calcium soaps Enzymatic fat necrosis(acute pancreatitis) Nonenzymatic fat necrosis (following direct trauma to adipose tissue & extracellular liberation of fat) 5/4/ /4/ Foci of fat necrosis with saponification in the mesentery. The areas of white chalky deposits represent calcium soap formation at sites of lipid breakdown. 5/4/ This is fat necrosis of the pancreas. Cellular injury to the pancreatic acini leads to release of powerful enzymes which damage fat by the production of soaps, and these appear grossly as the soft, chalky white areas seen here on the cut surfaces. 5/4/

13 Gangrene Extensive tissue necrosis Secondary bacterial infection Dry gangrene Wet gangrene Gas gangrene Microscopically, fat necrosis is seen here. Though the cellular outlines vaguely remain, the fat cells have lost their peripheral nuclei and their cytoplasm has become a pink amorphous mass of necrotic material. 5/4/ /4/ This is gangrene, or necrosis of many tissues in a body part. In this case, the toes were involved in a frostbite injury. This is an example of "dry" gangrene in which there 5/4/ is mainly coagulative necrosis from the anoxic injury. Toxic megacolon. Complete cessation of colon neuromuscular activity has led to massive dilatation of the colon and black-green discoloration signifying gangrene and impending rupture. 5/4/ Fibrinoid Necrosis A type of connective tissue necrosis Loss of normal structure A homogeneous,bright pink-staining necrotic material that resembles fibrin microscopically The small intestine is infarcted. The dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom. Some organs such as bowel with anastomosing blood supplies, or liver with a dual blood suppy, are hard to infarct. This bowel was caught in a hernia and the mesenteric 5/4/ blood supply was constricted by the small opening to the hernia sac. 5/4/

14 5/4/ Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name--fibrinoid necrosis. 恶性高血压病的肾脏小动脉 5/4/ Necrosis (5) Consequences of Necrosis Autolysis & inflammation Dissolution & absorption Sloughing Ulcer, Cavity, Sinus, Fistula Organization & encapsulation Calcification 5/4/ /4/ /4/ /4/

15 CHAPTER 1 Normal Adaptation Reversible Injury Irreversible Injury 5/4/ /4/