PATHOPHYSIOLOGY (PATHO) 370 FINAL EXAM STUDY GUIDE 2023 COMPLETE

PATHOPHYSIOLOGY (PATHO) 370 FINAL EXAM STUDY GUIDE 2023 COMPLETE. Etiology: study of causes or reasons for a particular injury. Idiopathic (unknown) vs Iatrogenic (unintended/unwanted medical treatment). Risk Factor: a factor that increases the likelihood of disease. 2. Pathogenesis: development or evolution of disease from initial stimulus to ultimate expression of manifestations of the disease. 3. Clinical Manifestations: Signs (objective) vs Symptoms (subjective). 4. Stages and Clinical Course: Latent period (time between exposure of tissue to injurious agent, first appearance of S&S), Prodromal period (indicating onset of disease), Acute phase (disease/illness reaches its full intensity). 5. Acute clinical course: short-lived, may have severe manifestations. 6. Chronic clinical course: may last months to years, sometimes follows an acute course. 7. Treatment implications: understanding the etiology, pathogenesis, and clinical consequences of a particular disorder/disease/illness may determine which treatments could be helpful. 8. Considerations: culture, age, gender, situation, time. 9. Levels of Prevention: Primary: altering susceptibility or reducing exposure for susceptible persons (vaccination). Secondary: early detection, screening, and management of disease. Tertiary: rehabilitation, supportive care, reducing disability, and restoring effective functioning. 10.Subclinical: disease that has no recognizable clinical findings. Distinct from a clinical disease which has S&S that can be recognized. Subclinical disease ex. Diabetes, hypothyroidism, RA until they turn into clinical diseases. Chapter 2: 1. Homeostasis: ideal set point; response: mechanistic, predictable series of orchestrated internal events. 2. Types of parameters to control: osmolarity, temperature, pH, nutrients, water, Na+, Ca2+, oxygen, hormones. 3. Allostasis: ability to adapt to challenges; maintains or reestablishes homeostasis in light of environmental and lifestyle changes. 4. Stressors: agents or conditions that endanger homeostasis (physical, chemical, emotional, biological, social, or cultural; vary in scope, intensity, and duration. 5. Feedback control systems adapt to changes to restore homeostasis. 6. Stress can be beneficial: increase energy and alertness, keeps us focused on the problem at hand. 7. Risk factors: NOT stressors, but conditions or situations that increase the likelihood of encountering a stressor. 8. Han Selye’s GAS: Alarm Reaction: arousal of CNS begins, fight-or-flight response sympathetic NS involved. Epinephrine, NE, and other hormones are released, causing an increase in HR, contractility, oxygen intake (respiratory rate), and mental activity. Resistance: activity of the nervous and endocrine systems in an attempt to return to homeostasis. Allostatic state: refers to the activity of various systems in attempting to restore homeostasis. Exhaustion: point where body can no longer return to homeostasis. Allostatic overload: “cost” of body’s organs and tissues for an excessive or ineffectively regulated allostatic response. Organ damage begins (onset of disease). 9. Other responses: corticotropin-releasing hormone (CRH) production, antidiuretic hormone release (vasopressin), Sympathetic nervous system (SNS) activation and catecholamines (E and NE), reninangiotensin-aldosterone pathway activation (increase BP, increased blood volume). 10.Stressful stimuli excite receptors which relay to the hypothalamus the stress response is then mediate by E/NE and glucocorticoids (cortisol). 11.SNS stimulation causes vasoconstriction of most blood vessels because of activation of alpha 1 Adrenergic receptor’s by NE. 12.Cortisol: stress hormone. Diverts metabolism from building tissues to supply energy to deal with the stress. Primary glucocorticoid. Promotes appetite. Causes S&S of chronic stress. Increased blood glucose, stronger sympathetic system effect on heart rate. *Hypothalamus (CRH)  Anterior Pituitary (ACTH)  Adrenal Cortex (cortisol)  alters glucose, fat, protein metabolism, suppresses inflammatory and immune responses. 13.Antidiuretic Hormone (ADH): vasopressin, causes vasoconstriction, makes kidneys reabsorb water from urine to blood. 14.Fight or Flight Response: rapid response to trauma, emergency. Epinephrine and norepinephrine released. Both attach to adrenergic receptors. Norepinephrine: causes vasoconstriction and raises BP, reduces gastric secretions, increases night and far vision. Epinephrine: enhances myocardial contractility, increases HR and CO, causes bronchodilation, increases glucose release from the liver (glycogenolysis).  Pain, fear, low BP (hypothalamus) SNS activated (SNS neurons)Norepinephrine (adrenal medulla)  epinephrine released into blood  heart (increase HR and contractility)/ Blood Vessels (vasoconstrict skin, gut, and kidney)  increased BP 15.Renin-Angiotensin-Aldosterone Pathway: activated by sympathetic system, decreased blood flow to kidneys. ANG1: weak vasoconstriction. Angiotensin-converting enzyme (ACE). ANG II: stronger vasoconstriction, also stimulates the adrenal cortex to release aldosterone. Aldosterone released. Na+/K+ ATPase in nephrons activated (kidneys reabsorb Na+ and H2O, kidneys secrete K+.  Kidneys release ReninConverts angiotensin to ANG I (ACE)ANG IIAdrenal CortexAldosteroneKidneysReabsorb Na+ and water (increases blood volume and BP) and secrete K+ 16.Endorphins: endogenous opioids- raises pain threshold and produces sedation and euphoria. 17.Oxytocin: produced during childbirth and lactation, associated with bonding and social attachment, thought to moderate stress response and produce a calming effect. 18.Stress Affects the Immune System: by decreasing immune cell production, decreasing thymus activity, overall stress and cortisol suppresses the immune system. 19.Types of Stress (1) Physiologic Stress: stress-induced changes in body functions, detected by body’s normal regulatory sensors, the body alters function to restore normal balance. When balance is restored, negative feedback stops the reaction. (2) Psychosocial Stress: refers to events of psychosocial or social origin which challenge homeostasis. Adverse environments or life experiences (natural disasters, war, loss of job). Position in a social hierarchy, isolation, discrimination. Directly affects the CNS. Turns on the stress responses, even when the body’s internal sensors have not detected imbalance. (3) Acute Stress: pounding headache, cold, moist skin, stiff neck. Activates neural pathways that mediate arousal, alertness, focused attention, aggression. Can be detrimental. (4) Chronic Stress: long term. sympathetic activity and cortisol are elevated, complications result from reduced immune response. Long-term exposure can lead to serious health problems because it disrupts most body systems. 20.PTSD: chronic stress, sympathetic system is activated, cortisol levels are decreased, due to life threatening events, less than half of people exposed to traumatic experiences suffer from PTSD. 21.PTSD 3 Symptoms: intrusion (flashbacks), avoidance (emotional numbing, depression), hyperarousal (increased irritability, increased concern over safety, difficulty concentrating. Memory problems, sleep disturbances, excessive anxiety. 22.Adaptation to Stress Determined By: physiologic reserve, time, health status, age, genetic endowment, hardiness, psychosocial factors, nutrition, sleep-wake cycle. 23.Tx of Stress Disorders: relaxation response, imagery, music therapy, massage therapy, biofeedback. Chapter 4: 1. Reversible Cell Injury Hydropic swelling: due to accumulation of water. 1st manifestation of most forms of reversible cell injury. Results from malfunction of NA+/K+ pump with accumulation of intracellular Na+. Any injury that results in loss of ATP will also result in swelling: Characterized by large, pale cytoplasm, dilated ER, swollen mitochondria, cells in organs increase in size and weight. Intracellular Accumulations: excess accumulations of substances. Leads to injury thru toxicity, immune response, taking up cellular space. Characterized by accumulation of excessive amounts of normal intracellular substance, abnormal substances from faulty metabolism synthesis, particles that the cell is unable to degrade. Common site of accumulation= Liver. 2. Cellular Adaptation Atrophy: cells shrink and reduce function, generally caused by ischemia, nutrient starvation, decreased functional demand, disuse, denervation, and persistent cell injury. Hypertrophy: increase in cell mass and augmented function capacity; generally caused by increased cellular protein content and increase functional demand. Hyperplasia: increase in functional capacity related to an increase in cell number due to mitotic division; caused by increase physiologic demand, hormonal stimulation, persistent cell injury, chronic irritation of epithelial cells. Metaplasia: replacement of one differentiated cell type with another. Fully reversible when injurious stimulate is removed. Dysplasia: disorganized appearance of cells because of abnormal variations in size, shape, and arrangement. Cause by adaptive effort to persistent injury gone astray. Significant potential to transform into cancerous cells. 3. Irreversible Cell Injury Necrosis: Cell death, usually due to ischemia or toxic injury. Occurs when injury is too severe. Pain, inflammation, loss of function, elevated serum of enzyme levels. Coagulative: most common, begins with ischemia, ends with degradation of plasma membrane. Liquefactive: liquefaction of lysosomal enzymes, formation of abscess or cyst from dissolved tissue (brain). Fat necrosis: death of adipose tissue, appears as chalk white area, usually due to trauma or pancreatitis. Caseous necrosis: characteristic of lung damage secondary to TB, resembles clumpy cheese. Gangrene: cellular death (necrosis) in a large area of tissue. Due to interruption of blood supply. Dry Gangrene: form of coagulative necrosis characterized by blackened, dry, wrinkled tissue separated by a line of demarcation from healthy tissue. Wet Gangrene: form of liquefactive necrosis, found in internal organs, rapidly fatal. Gas Gangrene: results from infection of necrotic tissue by anaerobic bacteria (Clostridium), characterized by formation of gas bubbles in damaged muscle tissue, can be rapidly fatal. Apoptosis: programmed cell death. Can occur in response to injury. Severe cell damage increased p53 (triggers cells death). Does not cause inflammation. 4. Ischemia: interruption of blood flow. Causes tissue hypoxia. Results in power failure in the cell. Most common cause of cell injury and injures cells faster than hypoxia alone. Disruption of O2 + accumulation of metabolic waste (lactic acidosis) = cell dysfunction. Can be reversible but not after plasma, mitochondria, and lysosomal membraned are damaged. 5. Nutritional Injury: not having adequate amounts of fats, carbs, proteins, vitamins, and minerals which are essential to normal cell function. May result from poor intake, altered absorption, inefficient cellular uptake, chronic alcoholism, poverty, acute/chronic illness. 6. Infectious/Immunologic Injury: bacteria and viruses. Added injury may occur indirectly b/c immune system was triggered. 7. Chemical Injury: toxic chemicals or poisons. 8. Physical/Mechanical Injury: abrupt change in ATM pressure, electricity, ionizing radiation, extreme change in temperature. 9. Cellular Aging: progressive decline in proliferation and reparative capacity of cells, exposure to environmental factors, DNA damage, accumulation of metabolic damage, inability to adapt. Chapter 7 1. Cancer: develop from a mutation in a single cell that grows without the control that characterized normal cell growth, do not die off, and may spread to other sites. 2. Neoplasia: “new growth” and implies abnormality of cellular growth. Can be both malignant or benign. 3. Tumor: a mass. Can be malignant or benign. 4. Malignant: cancer 5. Benign: can be easily cured. 6. Epidemiology: Men 1:2 risk, women 1:3 risk. 5-year survival rate: 66%. 1/3 of cancer deaths are attributed to lifestyle factors (tobacco, alcohol, sexual exposure, obesity). Additional risk factors: viruses, radiation, exposure, chemicals, genes, hormones, compromised immune system. 7. Tobacco Use: lung cancer (worst survival rate), pancreatic, kidney, bladder, mouth, esophageal, and cervical cancers. 8. Classification: classified by the tissue or cells it originates from Epithelial tissue: carcinomas Glandular tissue: adenocarcinomas Connective/Muscle/Bone tissue: sarcomas Brain tissue/Spinal Cord: gliomas Pigment cells: melanomas Plasma cells: myelomas Lymphatic tissues: lymphomas Leukocytes: leukemia Erythrocytes: erythroleukemia 9. Cell Cycle/Growth Factor Receptors: # of cells produced = # of cells that die. Cells divide only when told to by growth factors which cause stable cells to enter the. Cycle and divide. 10.Growth Factors: attach to receptors an often work by affecting the G proteins turning on enzymes and second messengers to signal the cell to divide. 11.Carcinogen: potential cancer-causing agent 12.Grading vs Staging: stage= describes the size of a tumor and how far it has spread. Grade=appearance of the cancerous cells. 13.Proto-oncogene: the normal genes that code for normal proteins used in cell division 14.Oncogenes: mutated proto-oncogenes (introduced by a retrovirus, lost/damaged DNA sequence, error in replication). * Still codes for the proteins needed for cell division but might produce too much protein, an abnormal protein, protein turns on/off by itself, protein that should be made by a different cell. 15.Tumor Suppressor Genes: form checkpoint tumor-suppressor proteins that usually stop division of mutated cells. Keep most mutations from developing into cancers. AKA cyclins/cyclin-dependent kinases. Low activity = more cancers. 16.Multistep Nature of Carcinogenesis: Initiation (initial mutation occurs)  Promotion (mutated cells are stimulated to divide)  Progression (tumor cells compete with one another and develop more mutations which make them more aggressive). 17.Differentiated cells: normal cells that are different from one another. When UNDIFFERENTIATED the cells rapidly divide and form malignant tumors. When DIFFERENTIATED the cells mutate and form benign tumors. 18.Benign Tumors: cells look like normal tissue cells and may perform the normal function of the tissues. May lead to over secretion. Usually have a capsule around them, do not invade neighboring tissues, but can damage nearby organs by compressing them. 19.Malignant Tumors: cells do not look like normal adult cells, do not perform normal functions of the organ, may secrete hormones of other tissues. No clear boundaries and send “legs” into surrounding tissue. Divide rapidly. Can compress and/or destroy surrounding tissues. Commonly produce telomerase (enzyme that repairs telomeres = basic immortality. 20.Metastasis: process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites. Cells in a primary tumor develop the ability to escape and travel in the blood. Occurs in 3 ways: circulation through the circulatory and lymphatic system, accidental transplantation during surgery, spreading to adjacent organs and tissues. 21.Manifestations of Cancer: a. Changes in organ function: organ damage, inflammation, failure, benign tumors may overproduce normal organ secretions, malignant tumors may cause overproduction, but more commonly decrease production of normal organ secretions. b. Nonspecific signs of tissue breakdown: protein wasting, bone breakdown c. Paraneoplastic Syndrome: consequences of hormones being secreted by tumor cells. d. Bone Marrow Suppression: contributes to anemia, leukopenia (low WBC), and thrombocytopenia (low platelets). e. Local effects of tumor growth: bleeding, compression of blood vessels, compression of lymph vessels (edema), compression of hollow organs, compression of nerves. (pain, paralysis). f. Cancer Cachexia: weight loss, generalized weakness, increased metabolic rate, loss of appetite, nausea/vomiting. g. Pain h. Immune System Suppression Chapter 10 1. Immune System 3 Functions: defend body against invasion or infection by pathogens (antigens), remove dead or damaged cells, attempt to recognize, remove abnormal cells (cancer cells). 2. 3 Lines of Defense: physical and chemical barrier to infection (skin, mucous membrane), inflammatory response, immune response (innate vs adaptive). 3. Innate Immunity: always present, requires no previous exposure. Non-specific (doesn’t distinguish), immediate response, involves NK cells and neutrophils/macrophages. 4. Inflammation: important part of innate immunity, increases vascular permeability, vasodilation, emigration of leukocytes, phagocytosis, chronic inflammation. 5. Inflammation Manifestations: redness, swelling, heat, pain, loss of function. 6. Purpose of Inflammation: neutralize and destroy invading agents, limit spread and prepare tissue for repair. 7. Adaptive Immunity: attacks specific antigens, slower response but more effective to 2nd exposure, involved B and T lymphocytes, includes cell-mediated/humoral immunity. 8. Stem cells: made in bone marrow. 9. B cells: mature in bone marrow. 10.T cells: mature in thymus. 11.Cell Mediated Immunity involves phagocytic cells that attack specific antigen, mediated by T lymphocytes. 12.Cytotoxic T Cells (CD8+): bind to surface of infected cells (MHC I), disrupt the membrane, and destroy before infecting other cells. 13.Helper T Cells (CD4+): stimulate B cells to mature into plasma cells which make antibodies. Stimulated by macrophages (MHC II) that display antigens. 14.Suppressor T Cells: reduce the humoral response. 15.Humoral Immunity: antibody proteins in the blood that attack the specific antigen, mediated by B lymphocytes. B lymphocytes can also become memory B cells which stay to fight future infections without needing a Helper T to tell them to. 16.Primary Immune Response: Macrophages eat antigen and present it to TH cells  TH cells activate B cells  B cells become plasma cells and produce antibodies  plasma antibody levels rise. *Can take 2-3 weeks, vaccination produces a primary immune response because B cells become memory cells. 17.Secondary Immune Response: B memory cells respond to antigen immediately  plasma antibody levels rise within days. Booster shots cause a secondary immune response so antibody levels will be high before the disease is encountered. 18.IgG: 80% of plasma antibodies. Is the major antibacterial/antiviral antibody, crosses placenta, smallest. Easily leaves bloodstream. 19.IgA: body secretions, protects against resp and GI infx. 20.IgM: first antibody produced during an immune response (primary), major antibody on B cells. 21.IgE: initiates inflammatory and allergic reactions. 22.IgD: found on surface of B cells with IgM, mainly acts as antigen receptor to stimulate B cells. 23.Excessive Immune Response: autoimmunity, hypersensitivity 24.Deficient Immune Response: absent or depressed 25.Autoimmunity: immune system. Recognized an individual’s own cells as foreign. Triggered by gender (f>m), chronic infx, stress, genetics. Tx of corticosteroids, tumor necrosis factor inhibitors that cause cell death, therapeutic plasmapheresis where components of disease is removed. 26.Hypersensitivity: normal immune response that is either inappropriately triggered, excessive, produces undesirable effects; usually does not occur on the first exposure. TYPES 1, 2, 3: mediated by antibodies produced by B lymphocytes. TYPE 4: mediated by. T cells and do not require antibodies. Type 1: allergic, strong genetic or hereditary linkage regarding IgE response. Mast cells and basophils are principle effector cells. Tx: antihistamines, beta-adrenergic (decrease bronchoconstriction), corticosteroids, anticholinergics (block parasympathetic), IgE therapy. (inhibits IgE binding to mast cells), Epinephrine (adrenergic agent). Type 2: tissue specific, cytotoxic, or cytolytic hypersensitivity. Occurs when antibodies attack antigens on surface of specific cells or tissues, causing lysis. Rh-neg MOTHER. Type 3: immune complex reaction. Immune/phagocytic systems fail to remove antigen-antibody immune complexes. Not tissue specific. Ex: lupus, immune complex glomerulonephritis. 27.Primary Immunodeficiency Disorders: may be congenital, genetic, or acquired. Are rare and often sex linked (X chromosome), suspected with recurring infx. 28.Secondary Immunodeficiency Disorders: caused by excessive or defective neuroendocrine responses. Excessive: increased corticosteroid increases infx susceptibility, Defective: low corticosteroid increases susceptibility to autoimmunity.