Summary PATHO FINAL EXAM STUDY GUIDE

PATHO FINAL EXAM STUDY GUIDEFor each disorder/condition listed below, please review: Categories or staging of disorder (when applicable) Main major (broad) topic (if not testing on disorder or disease) Signs and symptoms (clinical manifestations) Genetic considerations (when applicable) Risk factors: modifiable and non-modifiable Pathophysiologic changes Complications Laboratory/Diagnostic Testing (when applicable) • Cellular Changes – atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia o Atrophy: decrease in cell size ex: disuse, denervation, loss of endocrine stimulation, inadequate nutrition, ischemia, or decreased blood flow o Hypertrophy: increase in cell size, ex: exercise (normal), due to disease (abnormal) o Hyperplasia: increase in the number of cells, ex: breast and uterine enlargement in pregnancy (physiologic), regen of the liver after hepatectomy (compensatory), excess hormone stimulation, BPH, warts (nonphysiologic), o Metaplasia: reversible change in which one adult cell type is replaced by another adult cell type, ex: barrets esophagus in GERD o Dysplasia: deranged cell growth that results in cells that vary in size, shape, and organization, ex: dysplastic changes found during pap smear for cervical cancer • Causes, Mechanisms, and Consequences of the Stress Response, Cellular Injury & Cell Death o Causes of Cell Injury ▪ Injury from Physical Agents: common causes of injuries due to environmental exposure, occupational and transportation accidents, and physical violence and assault. • Mechanical Forces: injury or trauma due to mechanical forces as the result of body impact with another object • Extremes of Temps: extremes of heat and cold cause damage to the cell, its organelles, and its enzyme systems. • Electrical Injuries: can affect the body through extensive tissue injury and disruption of neural and cardiac impulses ▪ Radiation Injury Downloaded by DANIEL NDAMBIRI () lOMoARcPSD| Agradestuvia Page 2 of 38 Winter 2017 • Ionizing Radiation: impacts cells by causing ionization of molecules and atoms in the cell, by releasing free radicals that destroy cells, and by directly hitting target molecules in the cell. • Ultraviolet Radiation: cause sunburn and increase the risk of skin cancers. Skin damage produced is thought to be caused by reactive oxygen species and by damage to melanin-producing processes in the skin, also damages DNA resulting in the formation of pyrimidine dimers. • Nonionizing Radiation: includes infrared light, ultrasound, microwave, and laser energy. Exerts its effects by causing vibration and rotation of atoms and molecules which is eventually converted into thermal energy. ▪ Chemical Injury • Drugs: alcohol, prescription drugs, OTCs, and street drugs that are capable of directly or indirectly • Lead Toxicity: small amounts accumulate to reach toxic levels, and can come from flaking paint, lead-contaminated dust, and soil, root veggies, lead water pipes or soldered joints, pottery glazes, newsprint, and toys made in foreign countries. (anemia is a sign of lead toxicity) • Mercury Toxicity: vapor, inorganic divalent, methyl, and ethyl. Dental fillings (vapor), long-lived fish, tuna, and swordfish (methyl) ▪ Injury from biological agents: able to replicate and can continue to produce their injurious effects. Viruses, bacteria. ▪ Injury from nutritional imbalances: excesses and deficiencies. Obesity and diets high in sat fats predispose persons to atherosclerosis. Starvation, etc. can result in iron deficiency anemia, scurvy, beriberi, pellagra, and protein and calorie deficiencies. o Mechanisms of Cell Injury ▪ Free radical formation: highly reactive chemical species with an unpaired electron in the outer orbit of the molecule. The unpaired electron causes free radicals to be unstable and highly reactive so that they react nonspecifically with molecules in the vicinity. ROS are oxygen-containing molecules that include free radicals such as superoxide and hydroxyl radicals and nonradicals such as hydrogen peroxide. ▪ Hypoxia and ATP depletion: deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP. During Hypoxic conditions, hypoxia-inducible factors (HIFs) cause the expression of genes that stimulate red blood cell formation, produce ATP in the absence of oxygen, and increase angiogenesis (formation of new blood vessels). One important effect of reduced ATP is acute cell swelling caused by failure of the energy-dependent sodium/potassium pump which extrudes sodium from and returns potassium to the cell. With the impaired function of the pump, intracellular potassium decrease, and sodium and water accumulate in the cell. The movement of water and ions into the cell is associated with multiple changes including widening of the ER, membrane permeability, and decreased mitochondrial function. ▪ Disruption of intracellular calcium homeostasis: ischemia and certain toxins lead to an increase in cytosolic calcium because of increased reflux across the cell membrane and the release of calcium from intracellular stores. The increased calcium level may inappropriately activate several enzymes with potentially damaging effects. Injured cells accumulate calcium o Reversible Cell Injury and Cell Death Downloaded by DANIEL NDAMBIRI () lOMoARcPSD| Agradestuvia Page 3 of 38 Winter 2017 ▪ Reversible Cell Injury: Impairs cell function but does not result in cell death. Two patterns of reversible cell injury occur Cellular swelling: impairment of the energy-dependent Na+ /K+ ATPase membrane pump, usually as the result of hypoxic cell injury. Fatty change: linked to intracellular accumulation of fat ▪ Programmed Cell Death: Number of cells in tissues regulated by cell proliferation balanced with cell death. This process eliminates cells that: Are worn out, Have been produced in excess, Have developed improperly, and Have genetic damage. Cell death occurs via→ Necrosis, Apoptosis (programmed cell death) • Necrosis: Refers to cell death in an organ or tissue that is still part of a living person. Often interferes with cell replacement and tissue regeneration. Gangrene occurs when a considerable mass of tissue undergoes necrosis. • Gangrene: The term gangrene is applied when a considerable mass of tissue undergoes necrosis o Wet gangrene: Affected area: cold, swollen, pulseless, skin is moist, black, and under tension, blebs form on the surface, liquefaction occurs, and a foul odor is caused by bacterial action. The spread of tissue damage is rapid o Dry gangrene: Affected tissue: dry and shrinks, skin wrinkles, and its color changes to dark brown or black. The spread of dry gangrene is slow • Nomenclature of benign & metastatic tumors, mechanisms, and factors that contribute to cancer development, tumor growth, and tumor metastasis o Benign: Well-differentiated cells that are clustered together in a single mass, grow by expansion without invading surrounding tissues, and encapsulate. No Mets. o Malignant: Less well differentiated and can break loose, enter the circulatory or lymphatic system and form secondary malignant tumors at other sites (yes Mets), grows by invasion, and infiltrate surrounding tissues.