NURS 231/BIOD 331 Pathophysiology – Module 6 Exam – Latest 2025 Updated & Verified 100% Questions And Answers

NURS 231/BIOD 331 Pathophysiology – Module 6 Exam – Latest 2025 Updated & Verified 100% Questions And Answers physiology - ANSWER study of functional or physiologic change that result in a disruption of normal function physiology - ANSWER normal day to day function 2. pathology - ANSWER the directly observable lab study of cell and tissue changes associated with disease, study of observable changes 3. pathologist - ANSWER physician who looks for changes in cell and tissue health - ANSWER the state of an organism when it functions in homeostasis homeostasis - ANSWER state of equilibrium, what the body wants 4. negative feedback loop - ANSWER output of system acts to oppose changes from the input of the system, resulting stability 5. positive feedback loop - ANSWER output is unable to attenuate an input change resulting in an imbalance of system, often results in disease, heart failure - the body's response makes problem worse diagnosis - ANSWER signs and symptoms together signs - ANSWER what we see symptoms - ANSWER what patient tells us etiology - ANSWER causes of the disease, how did we get the disease 6. predisposing factors - ANSWER risk factors for developing a disease pathogeneisis - ANSWER process of beginning the disease, goes with etiology, what caused the start of the disease 7. syndrome - ANSWER compilation of signs and symptoms that point toward a diagnosis, AIDS - signs and lab work, compilation of signs and symptoms together insidious - ANSWER a gradual progression with very vague of mild signs prognosis - ANSWER how bad is it? what are the chances of recovery? 8. morbidity - ANSWER how many people have the disease, negatively affects quality of life mortality - ANSWER causes death epidemiology - ANSWER study of disease in a population 9. morbidity- ANSWER identifies disease before it shows signs and symptoms, cellular changes atrophy - ANSWER loss of growth, muscle growth diminishes hypertrophy - ANSWER increase in the size of individual cells 10. hyperplasia - ANSWER increase in the number of cells, healthy growth just more cells 11. metaplasia - ANSWER cell changes from one cell type to another. ciliated epithelial cells in smoker changes to regular cubodal cell dysplasia - ANSWER cells vary in size, shape and nucleus size/shape. less cell differentiation, precursor to cancer anaplasia - ANSWER cells lack differentiation, cancerous neoplasm - ANSWER new growth, malignant or benign idiopathic - ANSWER unknown cause iatrogenic - ANSWER caused by treatment, procedure or error 12. acute - ANSWER initial injury, localized chronic - ANSWER long term, less inflammation nosocomial - ANSWER hospital acquired infection 13. communicable - ANSWER ability to spread from one person to another sudden - ANSWER fast onset of disease prevalence - ANSWER how many have disease incidence - ANSWER how many have disease during a certain period of time hypoxia - ANSWER lack of oxygen 14. ischemia - ANSWER lack of blood flow, lack of oxygen and glucose to areas because of lack of blood flow, decreased ability to produce energy Necrosis/death - ANSWER cellular death, messy 15. Liquefaction necrosis - ANSWER tissue liquified by lysosomal enzymes coagulative necrosis - ANSWER dead tissue retains form 16. fat necrosis - ANSWER fatty acids are broken down and form soap caseous necrosis - ANSWER cheesy/curdled infarction/necrosis - ANSWER cellular death resulting from hypoxia gangrene - ANSWER an area of necrotic tissue which has been infected by bacteria exudate - ANSWER fluid collection at site of increased vascular permeability serous - ANSWER clear, yellow, fluid fibrinous - ANSWER high amounts of fibrin in fluid purulent - ANSWER many dead WBC, pus abcess - ANSWER walled off protected purulent exudate 17. hemmorrhagic - ANSWER blood in fluid, injury causes artery vein compromise dry gangrene - ANSWER result of coagulative necrosis wet gangrene - ANSWER neutrophils invade site causing liquefactive necrosis-found in internal organs gas gangrene - ANSWER caused by clostridium, destroy tissue, produce gas 18. necrotising fascitis - ANSWER infection in finger that runs under the skin following the fasci. Can lead to infection in other parts of body keloid - ANSWER hypertrophic scar tissue formation 19. contracture - ANSWER a permanent shortening of muscle or scar tissue that distorts or deforms (joints) 1st intention healing - ANSWER sutured, minimal amount of skin opening, small amount of granulation tissue, small scar, resolution-regeneration 2nd intention healing - ANSWER open healing, large wound, chronic wound, large area of granular tissue - large scar, repair acute inflamation - ANSWER localized, fever, high level of leukocytes 20. chronic inflamation - ANSWER longer than 10 days, less swelling and exudate than acute, more lyphocytes, more fibroblasts - larger scar formation anti inflammatory meds - ANSWER acetysalicylic acid, acetaminophen, NSAID, glucocorticoids Humoral Immunity - ANSWER B-cells and antibodies 21. IgG - ANSWER most abundant, pivotal in 2nd response, activator of Ag-Ab commpliment system IgM - ANSWER 1st responder, big, activator of Ag-Ab /commpliment system IgA - ANSWER tears, colostrum, secretions IgE - ANSWER release histamines, allergic response IgD - ANSWER bound to B-cells, antigen receptor 22. Cell Mediated (T/B cell) - ANSWER humoral-Bcells/antibodies, cell mediated T-cells Phagocytosis - ANSWER eat foreign material, present foreign material to the immune system 23. Complement System - ANSWER activate inflammatory response, plasma protein cascade activates and binds to Ag-Ab complex causing apoptosis Specific Immuntity - ANSWER humoral/cell mediated 24. Primary Immune Response - ANSWER humoral immunity dominated by IgM, smaller amounts of IgG Secondary Immune Response - ANSWER humoral response of large production of IgG 25. Passive Immunity - ANSWER borrow someone else's Ig, body does not have immune response, no memory B/T cells Active Immunity - ANSWER body undergoes immune response and makes B/T cells and stores memory cells 26. Natural Active Immunity - ANSWER immunity acquired through illness Artificial Active Immuntity - ANSWER immunity acquired through vaccination 27. Natural Passive Immuntity - ANSWER immunity acquired through placenta, colostrum Artificial Passive Immunity - ANSWER immunity acquired from antibodies produced from another organism, antivenin, rabies 28. Type I :Allergic Reactions - ANSWER allergies, anaphylaxis, histamine, can cause hypoxia - insect sting, antibiotics, foods, anesthetics Type II: Cytotoxic Hypersensitivity - ANSWER ABO incompatibility, IgG mediated donor blood destruction, inflammatory response, alloimmunity Type III: Immune Complex Hypersinsitivity - ANSWER Ag-Ab not removed by compliment, deposited in tissue, later compliment activation destroys tissue - serum sickness, rheumatic fever, autoimmune disorders - rheumatoid arthritis, MS, Lupus Type IV: Cell-Mediated/Delayed Hypersensitivity - ANSWER mediated by sensitized T-cells, delayed response, T-cell destroy tissue containing antigen, TB(mantoux test), contact dermatitis, poison ivy, graft host rejection/tissue rejection (alloimunity) 29. Anaphylactic Shock - ANSWER immediate body wide hypersensitive reaction 30. respiratory problems (burns) - ANSWER difficulty breathing, may have inhaled hot air and burned trachea physiology - ANSWER normal day to day function pathology - ANSWER the directly observable lab study of cell and tissue changes associated with disease, study of observable changes pathologist - ANSWER physician who looks for changes in cell and tissue health - ANSWER the state of an organism when it functions in homeostasis disease - ANSWER an interruption, cessation or disorder of body functions, systems or organs homeostasis - ANSWER state of equilibrium, what the body wants negative feedback loop - ANSWER output of system acts to oppose changes from the input of the system, resulting stability positive feedback loop - ANSWER output is unable to attenuate an input change resulting in an imbalance of system, often results in disease, heart failure - the body's response makes problem worse diagnosis - ANSWER signs and symptoms together signs - ANSWER what we see symptoms - ANSWER what patient tells us etiology - ANSWER causes of the disease, how did we get the disease predisposing factors - ANSWER risk factors for developing a disease pathogeneisis - ANSWER process of beginning the disease, goes with etiology, what caused the start of the disease syndrome - ANSWER compilation of signs and symptoms that point toward a diagnosis, AIDS - signs and lab work, compilation of signs and symptoms together insidious - ANSWER a gradual progression with very vague of mild signs prognosis - ANSWER how bad is it? what are the chances of recovery? morbidity - ANSWER how many people have the disease, negatively affects quality of life mortality - ANSWER causes death epidemiology - ANSWER study of disease in a population pathophysiology - ANSWER identifies disease before it shows signs and symptoms, cellular changes atrophy - ANSWER loss of growth, muscle growth diminishes hypertrophy - ANSWER increase in the size of individual cells hyperplasia - ANSWER increase in the number of cells, healthy growth just more cells metaplasia - ANSWER cell changes from one cell type to another. ciliated epithelial cells in smoker changes to regular cubodal cell dysplasia - ANSWER cells vary in size, shape and nucleus size/shape. less cell differentiation, precursor to cancer anaplasia - ANSWER cells lack differentiation, cancerous neoplasm - ANSWER new growth, malignant or benign idiopathic - ANSWER unknown cause iatrogenic - ANSWER caused by treatment, procedure or error acute - ANSWER initial injury, localized chronic - ANSWER long term, less inflammation nosocomial - ANSWER hospital acquired infection communicable - ANSWER ability to spread from one person to another sudden - ANSWER fast onset of disease prevalence - ANSWER how many have disease incidence - ANSWER how many have disease during a certain period of time hypoxia - ANSWER lack of oxygen ischemia - ANSWER lack of blood flow, lack of oxygen and glucose to areas because of lack of blood flow, decreased ability to produce energy Necrosis/death - ANSWER cellular death, messy Liquefaction necrosis - ANSWER tissue liquified by lysosomal enzymes coagulative necrosis - ANSWER dead tissue retains form fat necrosis - ANSWER fatty acids are broken down and form soap caseous necrosis - ANSWER cheesy/curdled infarction/necrosis - ANSWER cellular death resulting from hypoxia gangrene - ANSWER an area of necrotic tissue which has been infected by bacteria exudate - ANSWER fluid collection at site of increased vascular permeability serous - ANSWER clear, yellow, fluid fibrinous - ANSWER high amounts of fibrin in fluid purulent - ANSWER many dead WBC, pus abcess - ANSWER walled off protected purulent exudate hemmorrhagic - ANSWER blood in fluid, injury causes artery vein compromise dry gangrene - ANSWER result of coagulative necrosis wet gangrene - ANSWER neutrophils invade site causing liquefactive necrosis-found in internal organs gas gangrene - ANSWER caused by clostridium, destroy tissue, produce gas necrotising fascitis - ANSWER infection in finger that runs under the skin following the fasci. Can lead to infection in other parts of body keloid - ANSWER hypertrophic scar tissue formation contracture - ANSWER a permanent shortening of muscle or scar tissue that distorts or deforms (joints) 1st intention healing - ANSWER sutured, minimal amount of skin opening, small amount of granulation tissue, small scar, resolution-regeneration 2nd intention healing - ANSWER open healing, large wound, chronic wound, large area of granular tissue - large scar, repair acute inflamation - ANSWER localized, fever, high level of leukocytes chronic inflamation - ANSWER longer than 10 days, less swelling and exudate than acute, more lyphocytes, more fibroblasts - larger scar formation anti inflammatory meds - ANSWER acetysalicylic acid, acetaminophen, NSAID, glucocorticoids Humoral Immunity - ANSWER B-cells and antibodies IgG - ANSWER most abundant, pivotal in 2nd response, activator of Ag-Ab commpliment system IgM - ANSWER 1st responder, big, activator of Ag-Ab /commpliment system IgA - ANSWER tears, colostrum, secretions IgE - ANSWER release histamines, allergic response IgD - ANSWER bound to B-cells, antigen receptor Cell Mediated (T/B cell) - ANSWER humoral-Bcells/antibodies, cell mediated T-cells Phagocytosis - ANSWER eat foreign material, present foreign material to the immune system Complement System - ANSWER activate inflammatory response, plasma protein cascade activates and binds to Ag-Ab complex causing apoptosis Specific Immuntity - ANSWER humoral/cell mediated Primary Immune Response - ANSWER humoral immunity dominated by IgM, smaller amounts of IgG