NURS 5315 Advanced Pathophysiology Altered Cellular Function and Cancer Module Objectives with Advanced Organizers

NURS 5315 Advanced Pathophysiology Altered Cellular Function and Cancer Module Objectives with Advanced Organizers Cellular Adaptation Patterns 1. Analyze the differences between cellular adaptation patterns. a. Differentiate between the etiology and the pathophysiology of atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia and identify an example of each. Disease Etiology (cause by) Pathophysiology (causes) Example Atrophy An increase in catabolismos the intracellular organelles that causes a reduction of the structural components of the cell such as less mitochondria , myofilaments , and Physiologic atrophy occurs with early development Pathologic atrophy occurs due to decrease in workload, blood supply, nutrition, hormonal stimulation, and nerve stimulation Physiologic=thy mus gland shrinks during childhood Pathologic=skele ton muscle atrophy endoplasmic reticulum. Hypertrophy It is caused by hormonal stimulation or increased functional demand, which increases the cellular protein in the plasma membrane, endoplasmic reticulum, myofilaments, and mitochondria (not cellular fluid) Cardiomegaly, removing a kidney the other enlarges Hyperplasia (only cells that can undergo mitosis) Phy=Increas e rate of cellular division Path= can be caused by increased hormonal stimulation Phy=An increase in tissue mass after damage or partil resection. Path=Response to an injury if the injury has been severe or prolonged Liver regenerating, callus, uterus enlargement during pregnancy Dysplasia Due to persistent, severe cell injury or irritation Disordered cell growth. Epithelial tissue of the cervix and respiratory tract Metaplasia Cell exposed to chronic stressors, injury or irritation A stimulus induces a reprogramming of stem cells. The stem cell differentiates along a new cellular pathway. Barrett Esophagus b. Identify a physiologic and pathophysiologic example for atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia. Disease Physiologic Example Pathologic Example Atrophy Thymus gland bedrest Hypertrophy Skeletal muscles Cardiomegaly Hyperplasia Hormonal (uterus during pregnnancy0, liver regeneration Endometrium hyperplasia Dysplasia N/A Epithelial tissue of the cervix or respiratory tract Metaplasia Reverse back Bronchial metaplasia Mechanisms of Cellular Injury 2. Analyze the mechanisms and outcomes of cellular injury. a. Differentiate between the etiology, clinical manifestations and pathophysiology of cellular injuries caused by hypoxia, free radicals, and ethanol. Cellular Injury Etiology Clinical Manifestations Pathophysiology Hypoxic Injury ischemia The lack of oxygen Delivered to the cell causes a decrease in mitochondrial function. (? Inflamation) T his causes a decreased production of ATP and increases anaerobic metabolism (generating ATP from glycogen). Eventually anaerobic metabolism will stop and the cell will die. Free Radical and Reactive Oxygen Species have an unpaired electron in its outer shell unstable and highly reactive molecule ex Alzheimer’s PRK Ethanol metabolized to acetaldehyde in the cytoplasm of the cell. Liver and nutrition disorder seen mainly in the liver and stomach and are thought to be due to the generation of free radicals. b. Analyze the differences between the manifestations of oncosis, fatty infiltration, dystrophic calcification, metastatic calcification, urate accumulation and describe the implications for clinical practice. Cellular Injury Manifestation Cellular Effects Clinical Implications Oncosis Cellular swelling Hypoxic injury Fatty infiltration Accumulation of lipids (most commonly in the liver) ETOH, Fatty diet Dystrophic Calcification Accumulation of calcium in injured and dead tissue Tuberculosis, atherosclerosis, and heart valve disease Metastatic Calcification Mineral deposit in undamaged tissue due to hypercalcification Hyperthyroidism, toxic levels of vitamin D , addisons disease, hyperparathyroidism. Urate accumulation Deposition of urate in tissues, cell injury, and inflammation Acute arthritis, nephritis, chronic gouty arthritis c. Evaluate the process of necrosis, infarct, and apoptosis and describe the implications for clinical practice. Cell Death Cellular Effect Clinical Implications Necrosis Rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and the lack of typical features of apoptosis Coagulative necrosis happens in the kidney, heart, adrenal glands. Liquefactive necrosis happens in neurons and glial cells in the brain. Also caused by bacterial infections resulting in pus. Caseous necrosis occurs in lung tissue (combination of Coag & Liqu) Fat necrosis occurs in breast, pancreas, and abd structures. Caused by dissolution by lipases Gangrenous necrosis death of tissue due to hypoxia and subsequent bacterial invasion Infarct An area of necrosis from sudden insufficiency of arterial blood flow MI Apoptosis Self-destruction/programmed cell death Death by apoptosis causes loss of cells by -sever cell injury (injuried cell exceeds repaired cell -accumulation of misfolded proteins create mutations or free radicals which cause endoplasmic reticulum stree -infection -obstruction in tissue ducts d. Explain the five types of necrosis (coagulative, liquefactive, caseous, fat, gangrenous). Type of Necrosis Explanation Coagulative Coagulative necrosis: injury that occurs in the kidneys, heart, adrenal glands, and 2/2 hypoxia Liquefactiv e Liquefactive necrosis: 2/2 ischemic injuries that occur in nerve cells. Caseous Caseous Necrosis : injury occurs in lungs from TB Fat Fat Necrosis : breast, pancreas and other abd structures Gangrenous death of tissue due to hypoxia and subsequent bacterial invasion Altered Cellular Metabolism 3. Examine the mechanisms and effects of altered cellular metabolism. a. Analyze the steps of ethanol metabolism and describe how it causes hepatocellular damage. b. Analyze the main concepts of ketogenesis and describe the implications for clinical practice. Ketogenesis Concept Role Clinical implications Role of the hepatocytes Breaks down Acetul-CoA into three ketone bodies: Acetoacetate, Acetone, and B-hydroxybutyrate Role of the Ketogenesis mitochondria Triggers for ketogenesis Lack of glucose Role of Acetyl- CoA Returns to the citric acid cycle and combines with oxaloacetate to form citrate