PNUR 1700 Fall 2024 Week 2 Altered Cell Biology PDF

Week 2 Altered Cellular and Tissue Biology Cellular Adaptation Physiological (adaptive) versus pathogenic Atrophy Decrease in cellular size Hypertrophy Increase in cellular size Hyperplasia Increase in number of cells  Cellular...

Week 2 Altered Cellular and Tissue Biology Cellular Adaptation Physiological (adaptive) versus pathogenic Atrophy Decrease in cellular size Hypertrophy Increase in cellular size Hyperplasia Increase in number of cells  Cellular Adaptation (Cont.) Physiological (adaptive) versus pathogenic Dysplasia Deranged cellular growth Metaplasia Replacement of one type of cell with another Cellular Adaptation (Cont.) Cellular Adaptation (Cont.)  Occurs if cell unable to maintain homeostasis Cellular Reversible Cells recover Injury Irreversible Cells die Cellular Injury (Cont.) Cellular Injury Mechanisms Hypoxic injury Single most common cause of cellular injury Results from: Reduced amount of oxygen in the air Loss of hemoglobin or decreased efficacy of hemoglobin Decreased production of red blood cells Diseases of the respiratory and cardiovascular systems Poisoning of the oxidative enzymes (cytochromes) within the cells Cellular Injury Mechanisms (Cont.) Ischemia Most common cause of hypoxia Ischemia- Additional injury that can be caused by restoration of blood flow and oxygen Mechanisms: reperfusio Oxidative stress Increased intracellular calcium n injury Inflammation Complement activation Cellular Injury Mechanisms (Cont.) Anoxia Cellular responses: Decrease in ATP, causing failure of sodium–potassium pump and sodium– calcium exchange Cellular swelling Vacuolation Reperfusion injury Cellular Injury Mechanisms From Hausenloy, D.J., & Yellon, D.M.. Journal of Clinical Investigation, 123(1), 92–100.  Free radicals and reactive oxygen species (ROS) Cellular Injury Electrically uncharged Mechanisms atom or group of atoms having an (Cont.) unpaired electron that damage: Lipid peroxidation Alteration of proteins Alteration of DNA Mitochondria Reactive Oxygen Species Adapted from Kumar, V., Abbas, A.K., & Aster, J.C. [Eds.].. Robbins and Cotran pathologic basis of disease [10th ed.]. Saunders.  Chemical injury Xenobiotics Carbon tetrachloride Cellular Lead Injury Carbon monoxide Ethanol Mechanisms Mercury Social or street drugs (see Table 4.5)  Chemical agents including medications Over-the-counter and prescribed medications Leading cause of child poisoning Direct damage Cellular Chemicals and Injury medications injure cells by combining directly Mechanisms with critical molecular substances (Cont.) Chemotherapeutic medications Drugs of abuse Hypersensitivity reactions Range from mild skin rashes to immune- mediated organ failure Chemical Injury  Significant cause of morbidity and disability Blunt-force injuries Result of application of Unintentional mechanical force to body and Results in tearing, shearing, or crushing Intentional of tissues Motor vehicle Injuries accidents and falls Contusions Lacerations Fractures Unintentional and Intentional Injuries (Cont.) Sharp-force injuries Incised wound Stab wound Puncture wound Chopping wound Gunshot wounds Entrance Exit Range of fire  Asphyxial injuries: Caused by a failure of cells to receive or use oxygen Unintentional Suffocation Choking and asphyxiation Strangulation Intentional Hanging, ligature, Injuries and manual strangulation (Cont.) Chemical asphyxiants Cyanide and hydrogen sulphide Drowning Infectious Injury Pathogenicity of a microorganism Disease-producing potential Invasion and destruction Toxin production Production of hypersensitivity reactions Immunological and Inflammatory Injury Phagocytic cells Immune and inflammatory substances Histamine, antibodies, lymphokines, complement, and proteases Membrane alterations 1. What is the most common cause of cellular injury? A. Hypoxia B. Chemical injury from medications C. Free radical–induced D. Chemical injury from pollutants Manifestations of Cellular Injury Cellular accumulations (infiltrations): Water Lipids and carbohydrates Glycogen Proteins Manifestations of Cellular Injury (Cont.) Cellular accumulations (infiltrations) (cont.): Pigments Melanin, hemoproteins, bilirubin Calcium Dystrophic Metastatic Urate Systemic manifestations (see Table 4.10) Process of Oncosis (Hydropic Degeneration) Manifestations of Cellular Injury (Cont.) Calcium Infiltration Systemic Manifestations of Cellular Injury Manifestation Cause Fever Release of endogenous pyrogens (interleukin-1, tumour necrosis factor- alpha, prostaglandins) from bacteria or macrophages; acute inflammatory response Increased heart Increase in oxidative metabolic rate processes resulting from fever Increase in Increase in total number of white blood leukocytes cells because of infection; normal is 5 (leukocytosis) 000–9 000/mm3 (increase is directly related to severity of infection) Pain Various mechanisms, such as release of bradykinins, obstruction, pressure Presence of Release of enzymes from cells of cellular enzymes tissue* in extracellular fluid Lactate Release from red blood cells, liver, dehydrogenase kidney, skeletal muscle Systemic Manifestations of Cellular Manifestation Injury Cause (Cont.) Creatinine kinase Release from skeletal muscle, brain, heart (CK) (CK isoenzymes) Aspartate Release from heart, liver, skeletal muscle, aminotransferase kidney, pancreas (AST/SGOT) Alanine Release from liver, kidney, heart aminotransferase (ALT/SGPT) Alklaline Release from liver, bone phosphatase (ALP) Amylase Release from pancreas Aldolase Release from skeletal muscle, heart  Necrosis Sum of cellular changes after local cell death and the process of cellular autodigestion (autolysis) Coagulative Cellular Liquefactive Death Caseous Fat Gangrenous Gas gangrene  Coagulative necrosis Coagulative Kidneys, heart, and Necrosis adrenal glands Protein denaturation Coagulative Necrosis (Cont.) From Kumar, V., et al (Eds). (2015). Robbins and Cotran pathologic basis of disease (9th ed.). Elsevier.  Liquefactive necrosis Neurons and glial cells of the brain Liquefactive Hydrolytic enzymes Necrosis Bacterial infection Staphylococci, streptococci, and Escherichia coli Liquefactive Necrosis (Cont.) From Damjanov, I. (2012). Pathology for the health professions (4th ed.). Saunders.  Caseous necrosis Tuberculous pulmonary Caseous infection Necrosis Combination of coagulative and liquefactive necrosis Caseous Necrosis (Cont.) From Kumar, V., et al. (Eds.). (2021). Robbins and Cotran pathologic basis of disease (10th ed.). Elsevier.  Fat necrosis Breast, pancreas, and Fat Necrosis other abdominal organs Action of lipases Fat Necrosis (Cont.) From Damjanov, I., & Linder, J. (Eds.). (1996). Anderson’s pathology (10th ed.). Mosby.  Gangrenous necrosis Death of tissue from Gangrenous severe hypoxic injury Dry versus wet Necrosis gangrene Gas gangrene Clostridium Gangrenous Necrosis (Cont.)  Programmed cellular death Apoptosis Physiological versus pathological  Self-destructive and a survival mechanism Cytoplasmic contents delivered to lysosomes for Autophagy degradation Contributes to the aging process 2. Which type of necrosis best describes death of a cell from hypoxia, generally as a result of ischemia in the lower extremities? A. Fat B. Coagulative C. Liquefactive D. Gangrenous  Death of an entire person Postmortem changes: Somatic Algor mortis Death Livor mortis Rigor mortis Postmortem autolysis