Advanced Patho NURS 5315 exam 1

Advanced Patho NURS 5315 exam 1 action potential The process by which excitable cells transmit information from one to another. How is the action potential altered by a potassium imbalance? (Hyperkalemia) The ECF has more K+ ions. The membrane potential becomes more positive (hypopolarized). Cells become MORE excitable. T waves peak. QRS complexes widen. Causes dysrhythmias, weakness, paresthesia. {If membrane potential becomes equal to threshold potential cardiac standstill occurs} How is the action potential altered by a potassium imbalance? (Hypokalemia) The ECF has less K+ ions. The membrane potential becomes more negative or hyper-polarized. The cell becomes less excitable, depolarization takes longer, and takes a stronger stimulus. Causes weakness, atony, cardiac dystrhythmias. How is the action potential altered by a calcium imbalance? (hypercalemia) Increase in ECF calcium to 10.5 mg/dL. It decreases the cell permeability to calcium. The cell becomes hyperpolarized (the distance between membrane potential and threshold potential widens). The cell is less excitable and take more stimulus to depolarize. Causes: weakness, hyporeflexia, lethargy, confusion, shortened QT wave, depressed T wave. How is the action potential altered by a calcium imbalance? (hypocalemia) Decreased ECF calcium 9.0 mg/dL. 5.5 ionized. Increases the cell permeability to Na+. Resting membrane potential gets hypo-polarized. Cells become excitable and threshold and membrane potential get closer. Causes: tetany, hyperreflexia, parathesias, seizures, dysrhythmias. Atrophy Catabolism of intracellular organelles causing a reduction in the intracellular contents. The cell shrinks -The thymus gland shrinks in childhood -Disuse atrophy hypertrophy Hormonal stimulation in response to increased demand than causes an increase in cellular protien. The cell gets larger - eventually causing the whole organ to get larger. -Skeletal muscle hypertrophy in the weight lifter. -Cardiomegaly in response to hypertensive heart disease. Hyperplasia Increase in the number of growth factor cell receptors that activate cellular proliferation. Only happens in cell capable of mitosis. -Increased number of cells. -Uterine and mammary glands in pregnancy. -Increased production of endometrial cells due to estrogen/progesterone imbalance. Dysplasia abnormal changes in cell size, shape or organization in response to cell injury or irritation. Not a true adaptive process. -Cervical dysplasia. Metaplasia Mature cell type is replaced by a different mature cell type. -Reversible, but can induce metestatic change. -Result of chronic stressor to the cell. -Chronic smokers who loose normal ciliated epithelial cells (columnar) and the cells are replaced with squamous cells. -Barrett's esophagus: Normal esophogeal epithelial cells are replaced with columnar type cells that are more like the intestine to withstand the acidity of reflux. hypoxic injury Most common type of cellular injury. Caused by lack of oxygen, loss of hemoglobin, decrease in RBC production, cardiopulmonary disease, ischemia and inflammation. Causes mitochondrial disfunction ↓ decreased ATP production, ↑ anaerobic metabolism, metabolism ceases, cell dies. -Ischemia progresses to hypoxia. Causes intracellular enzymes to show up in labs. -Creatinine kinase - indicates muscle injury. -LDH - muscle, liver, lungs, heart, RBCs and brain. -AST - liver cells -ALT - liver cells -Troponin - heart Reperfusion injury Occurs when O2 supply is restored to ischemic tissues. Causes pH alterations. Trigger reactive oxygen intermediates to be produced causing cell membrane damage and mitochondrial calcium overload. Causes opening of MPTP allowing ATP to escape causing apatosis. Free radical and Reactive Oxygen Species Caused by a molecule with one unpaired electron. They will steal from another electron and cause that electron to become a free radical. ROS can overwhelm the mitochondria (they are a free radical subspecies) -Caused by endothelial injury and leads to atherosclerosis. -ROS have roles in Alzheimers, ALS, Parkinsons. ROS cause lipid peroxidation and destroy the cell membrane. Lipid peroxidation damages proteins and fragments DNA. Ethanol Mood altering CNS depressant. Causes nutrient deficiencies - Magnesium, B6, folic acid, thiamine, phosphorous. Causes inflammation, fatty liver, hepatomegaly and liver failure. -Metabolized by the liver to for acetyaldehyde in the cytoplasm of the cell. -Eventually causes lactic acidosis which prevents gluconeogenesis, increases triglycerides and heapatsteatosis. -Causes the utilization of Acetyl-CoA, causing ketoacidosis and hepatosteatosis. Necrosis Cell death from damage or injury. Rapid loss of cell membrane, organelle swelling, and mitochondrial dysfunction. -Leads to autolysis (complete autodigestion) Infarct Necrosis from sudden insufficient arterial blood flow. Apoptosis programmed cell death; normal death of cells that have completed their function and best serve the body by dying and getting out of the way Autophagy (self-eating) Key to cellular proliferation. When cells lack nutrition autophagy happens. Senescence Cessation of cellular proliferation Changes associated with aging -Accumulation of damaged macromolecules. -ROS accumulation -Progressive loss of tissues and organs over time. -Increased release of cytokines and proinflammatory substances. -Activation of the coagulation cascade that increases hyper-coagulability. -Binding of collagen - results in dehydration and wrinkling of skin. -Thymus atrophy. -Loss of ova in women. -Decreased spermatogenesis in men. -Decreased gastric emptying. -Muscle atrophy and sarcopenia. Ethanol metabolism Ethanol→acetylaldehyde→ acetyaldehyde dehydrogenase →acetate →oxidzed to Niacin (NAD+) →decreased NADH. The increased NAD+ to NADH ratio results in lactic acidosis, fasting hypoglycemia, elevated triglycerides, ketoacidosis, heaptosteatosis (fatty liver). Ketogenesis formation of ketone bodies. Ketones are formed in the absence of adequate glucose. {Mainly occurs in the mitochondria of the hepatocytes} Role of the hepatocytes in ketogenesis Liver cell where ketogenesis occurs. {Process acetyl-CoA into ketone bodies: acetoacetate, acetone and beta-hydroxybuturate} Role of the mitochondria in ketogenesis Where most of the ketogensis occurs. Triggers for ketogenesis Triggered by lack of glucose Clinical Implications: occur from the depletion of carbohydrate stores or may occur bc the cell is not able to use glucose but the individual is hyperglycemic (type 2 DM) Role of Acetyl-CoA in ketogenesis During glucose deprivation the cells do not produce energy. Acetyl-CoA is produced to turn fatty acids into energy. Acetyl-CoA produces 3 ketone bodies. Effect on oxaloacetate Used in gluconeogensis. During starvation and uncontrolled DM, Oxaloacetate is completely used up, leaving more Acetyl-CoA and therefore creation of more ketone bodies. Which causes ketoacidosis. Normal cell biology Grows from a stem cell - programmed to become a certain type of body cell. Cancer cell biology Grows unregulated. -Ignores signals to stop proliferating. -Can go undetected by the immune system. -Not encapsulated. Alpha-fetoprotein (AFP) - tumor marker hepatic, germ cell Carcinoembryonic antigen (CEA) - Tumor marker GI Pancrease Lung Breast Beta human chorionic gonadotropin - tumor marker germ cell choriocarcinoma prostate-specific antigen (PSA) - tumor marker Prostate Carcino- Epithelial tissue Hepatocellular carcinoma (epithelial tissue of the liver) Sarco- Connective tissue -Osteosarcoma (bone) -oma indicates tumor carinoma in situ Preinvasive Eary carcinoma of glandular or squamous epithelial tissue that has not broken through the basement membrane. -blastoma Nerve tissue -Neuroblastoma Lung cancer metastasis Brain Many organs Colorectal metastasis Liver Lungs Testicular metastasis Liver Lungs Brain Prostate Metastasis Bone (Lumbar vertebrae) Liver Breast metastasis Bone Lung Liver Brain Head and neck metastasis Lymphatics Liver Bone Ovarian metastasis Omentum pertioneal surfaces diaphragm liver Scarcoma metastasis Lungs