PATHOPHYSIOLOGY 370 FINAL EXAM STUDY GUIDE.

Chapter 1: PATHOPHYSIOLOGY 370 FINAL EXAM STUDY GUIDE 1. 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), renin- angiotensin-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/of f 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. Chapter 13 1. Total Blood Volume: 75.5 ml/kg in men, 66.5 ml/kg in women. 7%-8% of body weight. 5-6 L. Blood cells: 45% of blood volume, Plasma 55%. 2. Plasma: contains plasma proteins (serum albumin, globulin, fibrinogen) which are formed in liver, regulatory proteins (hormones, enzymes), organic constituents (products of tissue metabolism, nutritive organic materials), inorganic constituents (electrolytes, iron). 3. Transfusion reactions involve RBC destruction caused by recipient bodies. 4. Iron deficiency has low MCHC, MCH, MCV. 5. CO2 transported in the bloodstream as bicarbonate ion. 6. Bilirubin can detect excessive RBC lysis. 7. Blood Cells Erythrocytes (RBC): transport oxygen, remove CO2, buffer blood pH. Last 120 days b/c membranes become weakened, they have no nuclei so cannot make new membranes, and they break as the squeeze through capillaries. Leukocytes (WBC): act primarily in tissues but circulate in blood/lymph, form immune antibodies. Platelets: circulating fragments of megakaryocytes, form blood clots and control bleeding, 1/3 of platelets are in reserve in the spleen. 8. Adult Hemoglobin: 2 alpha chains, 2 beta chains; each chain hold a iron containing heme group that oxygen binds to. ~15 g of Hgb per 100 ml of blood. 9. Erythropoiesis: decreased blood oxygen, kidneys secrete EPO, bone marrow stimulated, created new red blood cells. 10. Spleen: houses WBC that are ready to process RBC’s, creating unconjugated bilirubin (toxic) from the hemoglobin. 11. Unconjugated Bilirubin:  turns into bilirubinemia  jaundice OR  liver links it to glucuronic acid  conjugated bilirubin  bile 12. Hemoglobinemia: build-up of Hgb in blood, makes plasma red. 13.Iron is NECESSARY for RBC production. 14. Hemoglobinuria: makes urine dark. Break in capillaries outside the spleen  release of Hgb into blood  Hemoglobinemia  Hemoglobinuria 15. Anemia: abnormally low Hgb level, number of RBCs, or both which results in low oxygen carrying capacity of the blood. Indication of some disease process or alteration in body function. 16. Compensatory Mechanism to restore tissue oxygenation: increased HR, CO, circulatory rate, flow to vital organs, increase in 2,3-DPG in RBC. 17. Causes of Anemia: blood loss, hemolysis, impaired RBC production. 18. Anemias: Iron-Deficient: most common Megaloblastic: inhibition of DNA synthesis in RBC production. Pernicious: lack of intrinsic factor from parietal cells which leads to B12 deficiency. Aplastic: stem cell disorder caused by bone marrow depression, caused by toxic, radiant, or immunologic injury to bone marrow. Leads to pancytopenia. Chronic: lack of EPO 19. Hemolytic Anemias: Membrane Disorder- Hereditary Spherocytosis: spherical rather than biconcave RBC’s (genetic). Acquired Hemolytic Anemias Hemolytic Disease of the Newborn: fetal RBC’s cross placenta and stimulate production of maternal antibodies against fetal RBC’s ***Glucose. 6 phosphate dehydrogenase deficiency, hemolytic anemia is most often triggered by bacterial or viral infections or by certain drugs. Hemoglobinopathies (inherited disorders): sickle cell, thalassemia 20. Thalassemia: genetic defect results in reduced rate of synthesis of one of the globin chains as well as increase hemolysis. Alpha: defective gene for alpha chain synthesis, may gave 1-4 defective genes, affects both fetal and adult Hb, in fetus gamma Hb may form, in adult beta HB may form. Beta: defective gene for beta chain, may have 1-2 defective genes, affects only adult Hb, alpha Hb may form. 21. Sickle Cell Disease: point mutation in beta chains of Hbg. When Hgb is deoxygenated the beta chains link together forming long protein rods that make cell sickle. Sickle cells. Cause vascular occlusion, pain, severe anemia, blocked capillaries, infarctions, jaundice. Tx is stem cell transplant. 22. Polycythemia: excess of RBC’s, increases blood viscosity and volume. - Polycythemia Vera: neoplastic transformation of bone marrow stem cells. - Secondary Polycythemia: due to chronic hypoxemia with resultant increase in EPO. - Relative Polycythemia: due to dehydration. 23.Fetal Hbg: CANNOT SICKLE b/c there is no beta chains. 24.Circulatory System FCN: deliver oxygen to the body tissues while removing carbon dioxide produced by metabolism. Chapter 14: 1. Hemostasis: arrest of bleeding or prevention of blood loss after blood vessel injury. Involves vessel wall, platelets, plasma coagulation proteins. 2. Hemophilia: inability to clot. prolonged bleeding time, prolonged aPTT (intrinsic, time it takes for blood to clot, determines if blood thinning therapy is effective), normal platelet count. 3. Vitamin K deficiency in newborns present with melena (GI), bleeding from the umbilicus, and hematuria 4. Vitamin K deficiency: normal bleeding time, normal platelet count, increase PT (extrinsic, prothrombin time: measures time for blood to clot) and INR (ensures that results from a PT test are the same from one lab to another). 5. Coagulation assessment: PT/INR, aPTT, bleeding time. 6. Aspirin thins blood so it can prolong bleeding time. 7. Cancer can cause thrombocytopenia because the bone marrow isn’t working normally and doesn’t make enough platelets. 8. Disseminated intravascular coagulation (DIC): condition in which blood clots form throughout the body, blocking small blood vessels. S&S of chest pain, SOB, leg pain, problems speaking. Usually caused by inflammation, infection, or cancer. 9. Dysfunction of the liver can lead to a clotting factor deficiency. Liver is in charge of synthesis of clotting and inhibitor factors, quantitative and qualitative platelet defects from liver disease. 10. Platelet normal count: 150k to 400 k. 11. Primary Hemostasis: initial response, vessel vasoconstricts to prevent blood loss and forms platelet plug. 12. Secondary Hemostasis: involves formation of a fibrin clot through intrinsic pathway (blood comes into contact with altered vascular endothelium) and extrinsic pathway (crush injury). Both pathways lead to prothrombin to thrombin, fibrinogen to fibrin (clot), called the coagulation cascade. 13. Final Stage: clot retraction 14. Thrombocytopenia: decreased thrombocytes, below 50k. Prolonged bleeding time, petechiae (pinpoint red spots), purpura (red or purple discoloration). Commonly caused by bone marrow suppression, immunization, alcohol ingestion. General Mechanisms- decreased platelet production, decreased platelet survival, splenic sequestration, intravascular dilution of circulating platelets. 15. Thrombocytosis: high platelet count, may bleed or clot, transitory (stress/physical exercise), primary (polycythemia vera or chronic granulocytic leukemia), or secondary (response to hemorrhage, disease process, or splenectomy. Chapter 15 1. Circulatory Circuit: absorption and delivery of nutrients, O2 uptake and delivery, waste removal 2. Lymphatic Circuit: specialized system of channels and tissues, reabsorbs fluid that leads from vascular network into the interstitial and returns to general circulation. 3. Thrombosis vs embolism: thrombus is a blood clot that forms in a vein. An embolus is anything that moves through a blood vessel until it reaches a smaller blood vessel. An embolus is often a small piece of a blood clot that broke off. 4. Arterial occlusions vs venous occlusions: arterial occlusions are commonly caused by atherosclerosis (fatty deposits inside a blood vessel), while venous occlusions are often the result of thrombosis (a blood clot in a blood vessel) 5. Peripheral edema is a result of venous thrombosis. 6. Artery Structure (inner to outer): tunica intimamediaadventitial 7. Vascular Endothelium: food and O2 pass into tissues, wastes and CO2 pass from tissues into blood, created compounds that cause constriction or dilation, creates growth factors that can stimulate smooth muscle, forms a smooth lining of the blood vessels that resist clot formation, created compounds that promote clot formation. 8. Arteriosclerosis/Atherosclerosis: hardening and loss of elasticity of the arteries. Athero is a type of arterio. Results from formation of fatty lesions in the intimal lining of large and medium sized arteries. Lipids get into vascular endothelium WBC try to clear away and cause foam cells  WBC and vascular endothelium release growth factors that promote plaque formation  plaque blocks the arteries. 9. Lipoproteins: the more protein, the higher the density 10. Atherosclerosis Develops: because a) scavenger cells encounter fatty deposits in the artery lining and try to destroy by oxidizing. Oxidized fats injure the endothelium, clots form and release growth factors, smooth muscle grows over the fatty core or b) tries to remove the fats by eating them and they become foam cells in the core of the plaque. 11. HDL: goes out into peripheral tissues and picks up lipids, then carry it back to the liver. 12. Aneurysms: localized blood-filled dilation of arterial vessels. Walls of artery weakens and stretches, risk of rupture and hemorrhage, risk of clot formation, frequently found in cerebral circulation and thoracic/abdominal aorta 13. DVT vs varicose veins: DVT are blood clots that form in the deep veins of the legs and may travel to lungs or cause a pulmonary embolism or blood clot in the lung because a part of the clot may break off. Varicose veins are superficial, large, swollen, and twisted veins caused by increased blood pressure in the veins. 14. True Aneurysm: involves all 3 layers of the artery wall. 15. False Aneurysm: a collection of blood leaking out of the lumen but confined next to the vessel. Chapter 16 1. Systolic BP: peak (higher) pressure, during systole. Reflects the amount of blood ejected with each beat (stroke volume) and compliance of the aorta and large arteries. Increases with age as the aorta and arteries lose elasticity. 2. Diastolic BP: lowest pressure, during diastole. Reflects closure of the aortic valve, the energy stored in elastic fibers of the large arteries, and the resistance to flow through arterioles into the capillaries 3. BP control involves both cardio and renal system: 4. Hypertension: increases morbidity and mortality with heart/kidney disease, stroke, peripheral vascular disease. 5. Primary/Essential Hypertension: idiopathic disorder, most common form; systolic blood pressure is a major risk factor for subsequent cardiovascular disease. Diuretics: decrease vascular volume, CO, and PR. B-adrenergic Receptor Blockers: decrease HR, CO, and renin release by kidneys. ACE inhibitors: inhibit conversion of ANG I to ANG II, therefore reducing ANG II’s effect on vasoconstriction and aldosterone levels. Angiotensin II receptor blockers Calcium Channel Blockers: decrease PR by inhibiting movement of Ca2+ into arterial smooth muscle. Central a2-adrenergic agonists: decrease sympathetic outflow. Central a1-adrenergic antagonists: cause vasodilation. Vasodilators: decrease PR. 6. Secondary Hypertension: attributed to specific identifiable pathology or condition. Accounts for only 5- 10%. Can be corrected or cured by surgery or treatment. 7. Hypertension Emergency vs urgency. Emergency: Systolic higher than 180 and/or diastolic higher than 120. Urgent: systolic higher than 140 or diastolic higher than 90. 8. Renal Hypertension: caused by decreased renal blood flow resulting in excessive release of renin, activating the RAA, causing peripheral vasoconstriction and sodium retention. 9. Hypotension Symptoms: fainting, nausea, dizziness, blurred/faded vision. Means that the heart, brain, and other parts of the body are not getting enough blood. 10. End organ damage of hypertension: heart- increased myocardial work resulting in heart failure, left ventricular hypertrophy, angina due to low blood flow. Brain- increased pressure in cerebral vasculature, hemorrhage, stoke, or TIA. Kidney- glomerular damage results in chronic kidney disease and failure. Peripheral vascular disease (PVD). Eyes: affects microcirculation of the eyes. 11. Adrenocortical Disorders: excess aldosterone and glucocorticoids (cortisol) production, increases sodium and water retention. 12. Blood Pressures: Normal: Less than 120 and less than 80 Elevated: 120-129 and less than 80 High Blood Pressure Hypertension Stage 1: 130-139 or 80-89 High Blood Pressure Hypertension Stage 2: 140 or higher or 90 or higher Hypertensive Crisis: higher than 180 and/or higher than 120 13. Coarctation of the Aorta: narrowing of the aorta, thus ejection of a large stroke volume into a narrow aorta causes increase in systolic BP. 14. Importance of Sodium in hypertension: higher amounts of sodium means more water retention which increases blood pressure. Water follow sodium, sodium goes into cell, the cell now has more water in it. 15. Action of ACE inhibitors: produces vasodilation by inhibiting the form of ANG II. This vasoconstrictor is formed by renin acting on circulating angiotension to form ANG I. Inhibitors prevent ACE enzyme from producing ANG II. ANG II would narrow the blood vessels and cause pressure to go up and heart to work harder. 16. Obesity/Obstructive sleep apnea 17. Complications of orthostatic hypotension: form of low BP that happens when you stand up from sitting or lying down. Can cause dizziness, faint. Can be caused by dehydration, low blood sugar, overheating. When you stand gravity causes blood to pool in your legs an abdomen which decreases blood pressure because there’s less blood circulating to the heart. Baroreceptors near the heart and neck usually send a signal to the brain which signals the heart to beat faster, pump more blood, which stabilizes BP. Can cause falls, stroke (bc of swings in BP), cardiovascular disease. Chapter 18 Right side • Blood enters the heart through two large veins, the inferior and superior vena cava, emptying oxygen-poor blood from the body into the right atrium. • As the atrium contracts, blood flows from your right atrium into your right ventricle through the open tricuspid valve. • When the ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts. • As the ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs where it is oxygenated. Left side • The pulmonary vein empties oxygen-rich blood from the lungs into the left atrium. • As the atrium contracts, blood flows from your left atrium into your left ventricle through the open mitral valve. • When the ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts. • As the ventricle contracts, blood leaves the heart through the aortic valve, into the aorta and to the body. 1. Disorders that affect the whole heart: pericardial disorders, coronary heart disease, myocardial diseases. Can cause symptoms of both right and left sided heart failure. 2. Pericarditis: inflammation of the pericardium, may restrict the hearts movement due to pericardial effusion (serous exudate filling the pericardial cavity; this may lead to cardiac tamponade: accumulation of exudate compressing the heart, causing reduced ventricular filling), or constrictive pericarditis (fibrous scar tissue makes pericardium stick to the heart). May cause ECG and pain. 3. Coronary Heart Disease: characterized by impaired coronary blood flow, usually result of atherosclerotic coronary arteries leading to cardiac ischemia. Also, through thrombus formation, coronary vasospasm, endothelial cell dysfunction. Divided into 2 types: chronic ischemic heart disease and Acute Coronary Syndrome (represents spectrum of ischemic coronary disease ranging from unstable angina through myocardial infarction). 4. Coronary Heart Disease: atherosclerosis blocks coronary arteries, ischemia. May cause angina, heart attack, cardiac arrythmias, conduction deficits, heart failure, or sudden death. 5. Chronic Ischemic Heart Disease: imbalance in blood supply and demand for oxygen. Less Blood (atherosclerosis, vasospasm, thrombosis); Higher oxygen demand (stress, exercise, cold). 6. Stable angina: pain when hearts oxygen demand increases. 7. Variant angina: pain when coronary arteries spasm. 8. Stable vs Unstable angina. Stable: during exercise/physical activity. Unstable: symptoms while resting. 9. Silent myocardial ischemia: oxygen is deprived to the heart. 10. Acute Coronary Syndromes: ECG changes (T wave inversion, ST segment depression or elevation, abnormal Q wave), Serum cardiac markers (proteins releases from necrotic cells: myoglobin, creatine kinase, troponin). 11. LDL and Heart Disease: LDL causes the build-up of fatty deposits in the arteries which reduced or blocks the flow. Of blood and oxygen to the heart. 12. Myocardial Infarction: chest pain (crushing, constrictive), SNS response (GI distress, nausea, vomiting, tachycardia, vasoconstriction, anxiety, restlessness, feeling of impending doom), hypotension and shock (weakness in arms and legs). 13. Complications of acute coronary syndrome: coronary arteries branch of f the aorta after it leaves the heart. Causes pumping problems due to MI, abnormal rhythms, pericarditis, blood clots, ventricular aneurysm. 14. Hypertrophic Cardiomyopathy: unusually thick ventricles, not enough room for blood to fill. Defects in contractile proteins make cells too weak. They hypertrophy to do the same amount of work as normal cells. Less space to fill with blood. Need more oxygen and perform less efficiently. 15. Restrictive cardiomyopathy: ventricles too stiff to stretch and fill. 16. MI, Myocarditis: ventricles are too weak to pump out blood due to inflammation of the heart. 17.Dilated Cardiomyopathy: Ventricles are too weak to pump out blood due to weakened, enlarged heart. 18.Peripartum Cardiomyopathy: Weak heart, final months of pregnancy. 19. MI tests: ECG, chest x ray, angiogram, ST elevation on ECG. 20. AV valves: Mitral (L) or tricuspid (R). 21.Semilunar: aortic (L) or pulmonary (R). 22. Heart Murmurs: valve defect, blood going through defective valves make noise; identify them by where they are, how they sound, when they happen. 23. Stenosis: valves do not open all the way; harder to force blood through. Will hear a murmur when the valve is open. 24. Regurgitant: valves do not close all the way; it leaks when it should be closed. Will hear a murmur when valve should be closed. 25. Mitral Valve Disorders (L): stenosis (narrowing), regurgitation (blood leaking), prolapse. 26.Aortic Valve Disorders (L): stenosis, regurgitation 27. Congenital Heart Defects: Atrial Septal Defect: allows blood flow between atrias. Ventricular Septal Defects: allows blood flow between ventricles. Endocardial Cushion Defects: no separation between the chambers of the heart. Coarctation of the aorta: narrowing of the aorta. Patent Ductus Arteriosus: the ductus arteriosus (which connects the aorta and pulmonary artery) remains open, allows blood to flow between the two vessels. Pulmonary Stenosis: pulmonary valve harder to open. Transposition of the great vessels: 2 major vessels that carry blood from heart (aorta/pulmonary artery) are switched. 28. Shunts: opening or connection that lets blood move from one side of the circulation to the other. Most shunts occur in the heart and move blood usually L to R because L side is stronger. 29. Shunts are normal before birth. 30. Foramen Ovale: blood goes from R to L atrium, bypassing the lungs 31. Ductus Arteriosus: blood goes from the pulmonary trunk to aorta, bypassing the lungs. 32.Ductus Venosus: blood goes from the visceral veins to vena cava, bypassing the liver. Chapter 19 1. Heart failure: impaired ability of the heart to pump blood to maintain sufficient CO to meet metabolic demands of tissues and organs. Results in congestion of blood flow in the systemic or pulmonary venous circulation. Most common reason for hospitalization in those >65 years of age. 2. Heart Failure: potential consequence of most cardiac disorders such as MI, high BP, degenerative conditions (cardiomyopathies), excessive work demands, volume overload 3. High-output Failure: supranormal output but inadequate due to excessive metabolic needs, anemia, arteriovenous shunting. 4. Low-output Failure: impaired heart pumping due to ischemic heart disease and cardiomyopathy. 5. Systolic Failure: impaired ejection of blood from the heart due to decreased contractility, volume overload, or pressure overload. 6. Diastolic Failure: impaired filling of heart due to smaller ventricular chamber size, hypertrophy, poor compliance. 7. Right-Sided Heart Failure: impairs ability to move deoxygenated blood from system to pulmonary circulation. Symptoms: awakening at night with SOB, SOB during exercise, coughing, wheezing, edema in ankles, legs, feet, abdomen, need to urinate, weight gain. 8. Left-Sided Heart Failure: impairs pumping of blood from the low-pressure pulmonary to the high-pressure arterial circulation. Fluid may back up in the lungs cause SOB< frothy sputum. 9. Adaptive Mechanisms to CO: SNS, RAA, Frank-starling mechanism, myocardial hypertrophy and remodeling. 10. Paroxysmal Nocturnal Dyspnea: sudden SOB during sleep. Symptom of COPD, pneumonia, heart failure. Heart failure occurs when heart muscle struggles to pump blood throughout body, can lead to fluid buildup in lungs aka pulmonary edema and make it difficult to breathe. 11. Frank-Starling Curve: the heart increases SV by increasing ventricular EDV, which increases myocardial fiber stretch to optimize actin and myosin overlap. (helps fibers stretch out to pump more blood). 12. Left-Sided Heart Failure: Right heart lungs fill with fluidLeft Heart (diastolic: does not accept enough blood from lungs)Systolic: LV does not pump enough blood to bodyBody lacks blood. 13. Right-Sided Heart Failure: Right heart (Systolic: RV does not pump enough blood to the lungs)Lungs (lungs do not oxygenate enough blood) left heartbody fikls with blood  Diastolic: RV does not accept enough blood from the body. 14. Pulmonary Edema: Capillary fluid moves into alveoli and lungs become stiffer, harder to inhale, less gas exchange, crackles, frothy sputum, Hgb not completely oxygenated. 15. CO and Heart Failure: to maintain CO the heart might increase HR or increase SV. If it can’t there will be backup of blood into the lungs, swelling in ankles, abdomen, low output symptoms such as fatigue, low urine output, lightheadedness. 16. Heart Failure Tx: relieve symptoms, improve QOL, surgical repair, Ace inhibitors, diuretics, B-adrenergic blocking agents, digitalis, restriction of salt intake, pacemaker. Chapter 20 1. Circulatory Shock: acute failure of circulatory system to supply peripheral tissue and organs of the body with an adequate blood supply, resulting in cellular hypoxia. Not a specific disease but can occur in the course of many diseases. 2. Pathogenesis: inadequate cellular oxygenation (from decreased CO, maldistribution of blood flow, reduced blood oxygen content), impaired tissue oxygenation results in cellular hypoxia which causes anaerobic metabolism, free radical production, macrophage induction, and failure of microcirculation to auto- regulate blood flow leads to activation of coagulation. 3. Compensatory Mechanism of Shock: homeostatic mechanisms are sufficient to maintain adequate tissue perfusion despite a reduction in CO, SNS activation attempts to maintain BP even though CO has fallen, progressive stage of shock is marked by hypotension and marked tissue hypoxia (lactate production increases with anaerobic metabolism, lack of ATP leads to cellular swelling, dysfunction, death, and cellular/organ dysfunction result from oxygen-free radicals, release of inflammatory cytokines, and activation of the clotting cascade). 4. Hypovolemic: loss of whole blood, loss of plasma, loss of extracellular fluid. Inadequate filling of vascular compartment and reduced venous return. Occurs when there is an acute loss of 15% to 20% circulating blood volume. Loss of plasma (severe burns), loss of whole blood (hemorrhage), loss of extracellular fluid (GI fluids lost in vomiting or diarrhea), dehydration. Tx: fluid replacement and control of source of volume loss. 5. Cardiogenic: alteration in cardiac function. Decreased CO lowers BP. SNS responds, vasoconstriction increases resistant to blood flow, increased workload on heart worsens heart failure. Usually a result of severe ventricular dysfunction due to myocardial infarction (MI, heart attack, loss of blood to heart), ineffective pumping caused by cardiac arrhythmias, ventricular septal defect, ventricular aneurysm, acute disruption of valvular function, problems associated with open heart surgery. Low CO= reduced oxygen delivery to tissues. Therapy aimed at improving CO and myocardial oxygen delivery, decreasing workload, inotropic, afterload reducing agents, intraaortic balloon counter pulsation, ventricular assist devices, heart transplantation. 6. Obstructive: inability of heart to fill properly, obstruction to outflow from the heart. Signs of right heart failure are seen. Common causes include pulmonary embolism, cardiac tamponade, tension pneumothorax. Rapid management of underlying obstruction is required to prevent cardiovascular collapse. EX: pulmonary embolism, cardiac tamponade. 7. Distributive: loss of sympathetic vasomotor tone, presence of vasodilating substance in the blood, presence of inflammatory mediators. Characterized by excessive vasodilation and peripheral pooling of blood. There is not enough blood to fill the circulatory system (CO inadequate due to reduced preload), blood flow decreases, less blood is returned to the heart, less blood is circulated to the body. Includes anaphylactic, neurogenic, septic. Caused by decreased sympathetic activity (neurogenic; brain or spine injury, insulin shock, emotion, drug overdose; Tx: vasopressors), vasodilator substances in blood (type 1 allergic hypersensitivity), inflammatory response to infection (sepsis), vessel damage from severe hypovolemia (decreased blood volume). 8. Anaphylactic Shock: result of excessive mast cell degranulation mediated by IgE antibodies in response to antigen. Mast cells release vasodilatory mediators resulting in severe hypotension (histamine, kinins, leukotrienes, prostaglandins), bronchoconstriction makes breathing more difficult. Clinical symptoms: hives, bronchoconstriction, stridor, wheezing, itching. Tx: maintenance of air way, epinephrine, antihistamines, vasopressors, and fluids. 9. Sepsis or Systemic Inflammatory Response Syndrome (SIRS): results from severe systemic inflammatory response to infection. Inflammatory mediators released into the circulation (tumor necrosis factor, interleukins, prostaglandins. Cause systemic signs of inflammation: fever and increased respiration, respiratory alkalosis, vasodilation, hypotension, increased capillary permeability with edema, warm flushed skin. Activate inflammatory pathways (coagulation, complement system). Tx: improve blood flow distribution and managing infection with antibiotics, fluids, improve cardiac and vascular performance. 10. Activated Protein C: drotecogin alfa- a recombinant form of activated protein C. Blocks clotting, blocks inflammation, increases survival of the most seriously ill sepsis patients, may cause bleeding. 11. Sepsis: caused by body’s response to infection. Body normally releases chemicals into the bloodstream to fight an infection. Sepsis occurs when the body’s response to the chemicals is out of balance and triggers changes that can damage multiple organ systems. 12. Complications of Shock: complications are inflammatory in nature, excessive immune response leads to leaking capillaries, damage from proteolytic enzymes, and systemic activation of the clotting and complement systems. 13. Acute Respiratory Distress Syndrome (ARDS): exudate enters alveoli and blocks gas exchange making inhaling more difficult, neutrophils enter alveoli and release inflammatory mediators that make pulmonary capillaries leaky; releases proteolytic enzymes, produce oxygen-free radicals. 14. Acute Renal Failure: renal vasoconstriction cuts off urine production (acute renal failure), continued vasoconstriction leads to hypoperfusion which cuts off renal oxygen supply, renal tubular cells die =acute tubular necrosis (ATN) associated with decreased excretion of waste products (creatinine, urea). 15. Multiple Organ Dysfunction Syndrome: most common causes (sepsis), initiated by immune mechanisms that are overactive/destructive, altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention, kidneys/lungs/liver/brain/heart, most frequent cause of death in noncoronary ICU, mortality rates vary 30-100%. Chapter 22 1. Airway: autonomic nervous system controls the diameter of the airways and consequently, resistance to airflow, via contraction and relaxation of smooth muscle. PNS = bronchoconstriction via vagus nerve and cholinergic receptors. SNS = bronchodilation via beta 2- adrenergic receptors. 2. Obstructive Pulmonary Disorders: manifested by increased resistance to airflow (difficulty exhaling). 3. Dry cough is a common sign of viral pneumonia. 4. Immunosuppression is a risk factor for active pulmonary TB. 5. Bacterial pneumonia S&S: productive cough, parenchymal infiltrates on x ray. 6. TB X Ray: ghon tubercle. 7. IgE: associated with inhaled allergens in asthma. 8. Allergic form of asthma: inflammation, mucosal edema, and bronchoconstriction 9. Alveolar destruction: caused by a lack of alpha anti-trypsin. 10.Recurrent infection can cause hypersecretion of mucus in chronic bronchitis. 11.All Obstructive Pulmonary Disorders: characterized by resistance to air flow. 12.Obstructions in lumen wall: asthma, bronchitis. 13.Obstruction from increasing pressure around outside of lumen: emphysema. 14.Obstruction of airway lumen: bronchiectasis, cystic fibrosis. 15. COPD leads to barrel chest due to air trapping. 16. Asthma: airway obstruction that is reversible, airway inflammation, increased airway responsiveness to a variety of stimuli. Most common chronic disease of children; genetics, eczema, African American risk factors. 17. Extrinsic Asthma (allergic): ½ of asthma cases. An IgE mediated response to specific antigens, with antibody production. Mechanism: IgE is produced in response to allergen exposure, bins to mast cells and cause the release of histamines, leukotrienes, prostaglandins, bradykinins, serotonin. Increased microvascular permeability, bronchoconstriction. Epithelial damage, smooth muscle, and mucous gland hypertrophy, mucus in lumen. 18. Intrinsic Asthma (non-allergic): no antibodies produced, caused by exercise, stress, aspirin, an exposure to pulmonary irritants (smoke, cleaning agents). These irritants cause usual asthmatic response of hypersensitive smooth muscles to constrict, airway inflammation and increased mucus production. 19. Asthma: common symptoms of wheezing, tight chest, dyspnea, cough, increased sputum production. Severe attacks use accessory muscles of respiration, intercoastal retractions, distant breath sounds with inspiration, orthopnea, agitation, tachycardia, tachypnea. TX: avoid triggers, air purifiers, remove allergens, desensitization, oxygen therapy, corticosteroids, mast cell inhibitors. 20. Chronic Bronchitis: form of COPD where there is persistent narrowing of the airway due to chronic inflammation, scarring, and excessive mucus production. Chronic or recurrent productive cough lasting more than 3 months per year for 2 or more years. Damage not reversible. Type B COPD Blue Bloaters. Caused by cigarette smoke, rpt airway infx, genetics, inhalation of irritants. Pathogenesis: chronic inflammation/swelling of bronchial mucosa resulting in scarring, hyperplasia of bronchial mucous, increased bronchial wall thickness, pulmonary hypertension. SOB, excessive sputum, cyanosis, polycythemia, excessive body fluids. Tx: bronchodilator therapy, remove secretions, prevent muscle fatigue, low dose oxygen. **LEADS TO COR PULMONALE DUE TO INCREASED PULMONARY VASCULAR RESISTANCE. Thick mucus, fibrosis, and smooth muscle hypertrophy are parts of airway obstruction in CB. Also common to see chronic cough. 21. Emphysema: destruction of alveoli and small airways due to release of proteolytic enzymes from immune cells, occurs in smokers, Type A COPD or pink puffers. Common in mining, welding, asbestos. Pathogenesis: alveolar destruction is due to release of inflammatory cells (neutrophils, macrophages) that degrade lung proteins. Smoking also inhibits a protective enzyme, a1-antitrypsin, that normally keeps proteolytic enzymes in check. Genetic a1-antitrypsin is an uncommon cause of emphysema. Loss of elastic tissue in lungs. 22. Emphysema Respiratory Problems: a decrease in surface area for gas exchange, airway collapse due to loss of radial traction. Manifests as dyspnea, weight loss, use of accessory muscles to breathe, a low/flat diaphragm, barrel chest, pursed-lip breathing, leaning forward to breath, cough, cyanosis. Tx: cessation of smoking, oxygen therapy. 23. Acute asthma attack: associated with wheezing, coughing, chest tightness, use of accessory muscles. Complication: status asthmaticus 24. Pink Puffers: usually emphysema; by sustaining high ventilatory effort, a patient can have blood oxygen levels that are generally maintained near normal. SOB, increased ventilatory effort, use accessory muscles, pursed-lip breathing. 25. Blue Bloaters: cannot increase respiration enough to maintain oxygen levels, cyanosis (blue skin) and polycythemia, cor pulmonale (change in RV of heart due to respiratory disorders). 26. Bronchiectasis: aneurysm-like dilation of the bronchioles. Bronchiolar dilations serve as pockets of infection, producing foul-smelling sputum. Pathogenesis: recurrent infection of bronchial wall leads to persistent dilation, recurrent inflammation results in destruction of wall, destruction process leads to loss of ciliated epithelium. Chronic, productive cough, digital clubbing, treatment centers on antibiotic therapy and removal of secretions. Tx: remove secretions, abx. 27. Cystic Fibrosis: autosomal recessive disorder of chloride and water transport proteins affecting exocrine glands and mucus cells. Leads to dehydration and mucosal thickening in the respiratory and intestinal tract. Thick mucus secretions cause airway obstruction and air trapping. Obstructs pancreatic and biliary ducts. Tx removal of secretions, abx therapy. Chapter 23 1. Restrictive Pulmonary Disorders: category of respiratory diseases characterized by a loss of lung compliance, resulting in decreased lung expansion and increased lung stiffness. Causes include alterations in lung parenchyma (alveoli, bronchioles), pleura, chest wall, neuromuscular function. Characterized by decrease in VC, TLC, FRC, and RV. The greater the decrease in lung volume, greater the severity of disease. Decreased PaO2, normal or decreased PaO2, increased pH (alkalosis). 2. ARDS: characterized by hypoxemia. 3. Occupational Lung Diseases: result from inhalation of toxic gases or foreign particles, atmospheric pollutants have large effect. 4. Pneumoconiosis: caused by inhalation of inorganic dust particles, greater the exposure the worse it gets. 5. Pneumothorax (collapsed lung): air leaks into space between lung/chest wall, air pushes on the outside of lung making it collapse. Characterized by tracheal shift and respiratory distress. Air that enters the pleural space during inspiration but is unable to exit during expiration leads to tension pneumothorax. 6. Pneumothorax and ARDS: types of restrictive respiratory disorders. 7. Anthracnosis: coal miner’s lung or black lung 8. Silicosis: silica inhalation 9. Interstitial lung disease: honeycomb appearance, immunological in nature, and loss of alveolar walls. 10.Asbestosis: asbestos inhalation 11. Pathogenesis of all: pollutants interfere and. Paralyze cilia resulting in impaired clearance effect and inability to remove mucus/dust/foreign particles, etc. Alveolar macrophages try to engulf and remove particles by secreting lysosomes. Secreted enzymes damage alveolar wall causing deposition of fibrous material. 12. Clinical Manifestations: pneumoconiosis produces no S&S in early stage, progressive cough, dyspnea, cor pulmonale, resp failure, chronic hypoxemia. 13. TX: preventative measure, corticosteroids, bronchodilators, oxygen therapy, ventilator, deep breathing. 14.Sarcoidosis: presence of CD4+ cells, non-productive cough, granulomas, fatigue, weight loss, and fever. 15. Pleural Effusion: “water on the lungs” characterized by dyspnea, diminished breath sounds, and tracheal shift. 16. Pickwickian Syndrome: increased abdominal size forces thoracic contents upward into chest cavity, decreases lung expansion and diaphragmatic shortening. Chest Wall deformity. 17. Sleep Apnea Syndrome: soft tissue deposits in neck and predispose person to upper airway obstruction. 18.Obese Chest Wall Deformities Manifestations: decreased alveolar ventilation, hypoxemia, sleepiness, SOB, polycythemia, cor pulmonale, impotence, headache. 19.TX: oxygen therapy, caloric intake energy deficit, aerobic exercise, gastric bypass or stapling. Chapter 24 1. Abnormalities in Body Fluid: can occur in volume, concentration, electrolyte composition of body fluid. 2. Extracellular fluid: contained outside cells. 3. Interstitial: between cells, rich in Na, Cl, HCO3, and proteins. 4. Magnesium-aluminum antacids are a risk factor for hypophosphatemia 5. Vascular compartment: in blood vessels, rich in proteins. 6. Intracellular fluid: contained inside cells, rich in K, Mg 2+, inorganic and organic phosphates, and proteins. Low in Na and Cl. 7. Hyperparathyroidism is a risk factor for hypercalcemia. 8. Hypocalcemia and hypomagnesemia both increase neuromuscular excitability. 9. Vomiting (emesis) can cause metabolic alkalosis. 10.Diarrhea can cause metabolic acidosis. 11.Hypernatremia: confusion. 12. Hypokalemia: muscle weakness, cardiac dysrhythmias are manifestations of moderate to severe hypokalemia. 13. Chronic alcoholism: cause for hypomagnesemia. 14. Decreased ADH can cause hypernatremia 15. Hyponatremia: characterized by confusion, lethargy, coma, seizures. 16. Kidneys: fluid balance regulates the amount and makeup of body fluids, ADH from pituitary- reabsorb water, aldosterone- reabsorb Na+, secrete K-. Acid Base balance: secrete and reabsorb H+ and HCO3. 17. High osmolarity causes thirst which increases water intake, ADH release which reabsorbs from urine. 18.Low osmolarity causes lack of thirst and decreased ADH release so water is lost in urine. 19. Sodium: 135-145 mEq/L. Regulates extracellular fluid volume and osmolarity. 20. Potassium: 3.5-5.0. mEq/L. Maintains intracellular osmolarity, controls cell resting membrane potential, needed for Na K pump, exchanged for H. to buffer changes in blood pH, KH exchange occurs in the tissues and in the distal tubule of the nephron. 21. Cell Firing: stimulus: some Na channels open; at threshold more Na channels open, rushing in, making the cell positive (depolarizing); action potential: cell responds, contracts. K channels open making the cell negative again (repolarization), Na K pump removes the Na from the cell and pumps the K back in. 22. Hyperkalemia: raises resting potential toward threshold. Cells fire more easily, if resting potential reaches threshold, Na gates open and won’t close. 23. Hypokalemia: lowers resting potential away from threshold, cells fire less easily. 24. Calcium: 9-11 mg/dL, 4.5-5.5 mEq/L. Extracellular: blocks Na gates in nerve and muscle cells, clotting, leaks into cardiac muscle, causing it to fire, intracellular: needed for all muscle contraction, acts as second messenger in many hormone and neurotransmitter pathways. 25. Hypercalcemia: blocks more Na gates, nerves are less able to fire. 26.Hypocalcemia: blocks fewer Na gates, nerves fire more easily. 27. Magnesium: 1.5-2.5 mEq/L. Cofactor in ATP, DNA replication, mRNA production. 28. Normal pH: 7.35-7.45, cellular function is impaired when pH of body fluids becomes abnormal. H blocks Na gates. 29. Relationship between metabolic alkalosis and hypokalemia: due to low extracellular potassium concentration potassium shifts out of cells. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. 30. Headaches are an early sign of metabolic acidosis. 31. Regulators of Acid-Base: Buffers- chemicals that prevent large changes in pH by releasing or taking up H, mostly HCO3, normal ratio of bicarbonate to carbonic acid is 20:1, any deviation alters blood pH. Respiratory System: hyper/hypoventilation alters Co2. Renal system: excretes or retains metabolic acids. 32. Hyperventilation can cause respiratory alkalosis. 33.Hypoventilation is compensatory mechanism for metabolic alkalosis. 34.Respiratory Acidosis: increased Co2, increased carbonic acid, increased H (low pH), increased bicarbonate 35.Respiratory alkalosis: decreased CO2, decreased carbonic acid, decreased H (high ph), decreased bicarbonate. 36. Metabolic Acidosis: increased metabolic acids which raised H and lowers pH, decreased bicarbonate. 37.Metabolic Alkalosis: decreased H which increased pH, increased bicarbonate. Chapter 27, 29 1. S&S of Kidney Stones: differ in their size and location. Acute renal colic pain (intermittent sharp pain) or flank pain (stones within the kidney). Pain associated with nausea, vomiting, diaphoresis, tachycardia, and tachypnea. Once stone reaches bladder there is a reduction in pain 2. Common Composition of Renal Calculi: calcium. Urine becomes too saturated with specific solute, then form crystals if the concentration is too great (supersaturation). Usually begin development in the nephron and kidney pelvis. Crystallization is enhanced when a person is dehydrated or has high levels of solute in the kidney from excessive excretion (calcium, uric acid). Calcus matrix consists of protein, sugar, glucosamine, bound water, and organic ash. 3. Polycystic Kidney Disease: 4. Glomerulonephritis: inflammation of the glomeruli that results in chronic renal failure. Activated complement attracts neutrophils and monocytes. They release lysosomal enzymes that damage the glomerular cell walls. This increases permeability, and the loss of negative charge. Results in enhanced protein filtration, all affecting GFR. Most common in boys age 3-7. 5. S&S of Renal Cancer: 6. Uric acid crystals in renal calculi from gouty arthritis: 7. Hematuria is the most frequent and initial symptom of bladder cancer. 8. Vesicoureteral reflux (backup into the ureters) can lead to recurrent cystitis. 9. E coli is the cause for majority of UTIs. 10.Sexually active women are more prone to TI. 11.Ureterocele is a cystic dilation of the ureter. 12.Smoking is a risk factor for bladder cancer. 13. Stress vs urge incontinence. STRESS: weakening of or damage to the muscle used to prevent urination (pelvic floor and the urethral sphincter). URGE: result of overactivity of the detrusor muscle which controls the bladder 14. Characteristics of cystitis: mucosal inflammation and congestion. The detrusor muscle of the bladder becomes hyperactive, decreasing bladder capacity and leading to reflux into the ureters. This transient reflux can cause acute or chronic pyelonephritis if the bacteria ascends to the kidney. 15. Function of the kidneys: regulation of extracellular fluid volume and blood pressure, regulation of osmolarity, maintenance of ion balance (especially Na+, K+, and Ca2+), homeostatic regulation of pH (removal or conservation of H+ or HCO3 - ), excretion of wastes, production of hormones (synthesize erythropoietin (regulates RBC synthesis) (synthesize renin (regulates hormones involved in sodium balance and BP homeostasis). 16. UTI: common bacterial infections that enter through the urethra or bloodstream ● Bacterial infections include: ● E. coli ● Staphylococcus ● Can occur in the upper or lower urinary tract ● Upper UTIs are more serious because they can cause renal damage. 17. UTI Risk Factors: urinary obstruction and reflux (urine from urethra move back into bladder, or bladder into ureters; results in urine remaining in the bladder and acts as a medium for microbial growth), neurogenic disorders that impair bladder emptying, sexually active women, postmenopausal women (estrogen i