CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY, Exams of Nursing

Download CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY and more Exams Nursing in PDF only on Docsity! CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Absorb- take in or soak up Ccute- has relatively severe manifestations but runs short course measured in hours, days, or a few weeks. Adverse- preventing successes or development; harmful Chronic- lasts for months to years. Clinical- relating to the observation and treatment of actual patients rather than theoretical or laboratory studies Manifestations- are observed as signs of diseases, both objective and subjective Compensate-to give something in recognition of loss/injury cyanosis- a bluish discoloration of the skin resulting from poor circulation or inadequate oxygen to the blood. Cytology- the branch of biology surrounding the structure of plant and animal cells Detrimental- tending to cause harm Disseminate- spread widely Diagnosis- the identification of the nature of an illness by examination of symptoms Endemic- a disease or condition regularly found among a particular people in a certain area Epidemic- a disease is disseminated to many individuals at the same time Epidemiology- the study and analysis of the distribution and patterns of health and disease conditions in defined populations Etiology- the study of causes or reasons for a phenomena Exacerbate- to make worse Excrete- to separate and expel as waste Histology- the study of microscopic structure of tissues Hypoxemia- poor oxygenation of blood Hypoxia- a condition in which the body is deprived of adequate oxygen supply Iatrogenic- the cause is a result of an unintended or unwanted medical intervention Idiopathic- the cause is unknown Incidence- the occurrence, rate, or frequency of a crime incubation period- the interval between exposure of a tissue to an injurious agent and the first appearance of symptoms in the case of infectious diseases. Infarction- death tissue due to inadequate blood supply to the affected area Inhibit- to hold in/hold back, restrain Insidious- proceeding a gradual, subtle way, but with harmful effects Intermittent- occurring at irregular cycles Ischemia- inadequate delivery of blood to cells Latent period- the interval between exposure to a tissue to an injurious agent and the first appearance of symptoms CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Maladaptive- dysfunctional Morbidity- the condition of being diseased Mortality- the state of being subject to death Multifactorial- involving or dependent on a number of factors or causes Occlusion- the blockage or closing of a blood vessel or hollow organ Occurrence- an event/incident Pallor- an unhealthy appearance Pandemic- are epidemics that affect large regions and perhaps spreading worldwide Pathogenesis- refers to the development or evolution of a disease Pathology- the study and diagnosis of disease through examination of organs, tissues, cells, and bodily fluids Pathophysiology- the disordered physiological processes associated with disease/injury Perfusion- the passage of blood through the blood vessels or other natural channels Physiology- the branch of biology that deals with live organisms and their parts Prevalence- commonness Prodromal period- the appearance of the first signs and symptoms indicating the onset of disease Prognosis- the forecast of what is likely to come of the disease Prolonged- extend the duration of Remission- a temporary recovery Risk factor- when the link between an etiologic factor and development of disease is less than certain but the probability is increases when the factor is present Secrete- produced and discharged Sensitivity- the ability of an organism to respond to external stimuli Sequelae- a condition that is the consequence of a previous disease/injury Signs- abnormalities that signify a potential medical condition Specificity- the range of a function in which the antibody is effective Subclinical stage- during which the patient functions normally, although the disease processes are well established Symptoms- abnormalities that signify a potential medical condition Syndrome- a set of medical signs that correlate with each other and associates with a particular disease Transient- lasting only for a short time CHAPTER 2: HOMEOSTASIS AND ADAPTIVE RESPONSES TO STRESSORS CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • ACTH causes adrenal cortex to release glucocorticoids o Regulate steroid hormone cortisol by releasing it o Produced in the pituitary gland in the brain - role of posterior pituitary and function of antidiuretic hormone/vasopressin (ADH) - role of adrenal glands and functions of: • Posterior pituitary o The back portion of the master gland o Secretes oxytocin which increase uterine contractions and ADH • ADH o Increases reabsorption of water by tubules in the kidney - catecholamines – epinephrine, norepinephrine • Catecholamines o Release of is imitated through the activation of the hypothalamus gland • Epinephrine o Increases glycogenolysis (release of glucose from the liver and inhibits insulin secretion, elevating blood glucose levels) o Enhanced myocardial contractility and increases heart and cardiac output • Norepinephrine o The primary constrictor of smooth muscle in blood cells and regulate blood flow through tissues and its distribution to organs, maintaining blood pressure o Reduces gastric secretion, inhibits secretion, and innervates muscles of the eyes, dilating pupils and increasing night and far vision - corticosteroids – cortisol, aldosterone • Corticosteroids/glucocorticoids o Lipid-soluble hormones; practically every tissue in body has receptors CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Onset is slower and duration longer o Significant role in the control of the immune system • Cortisol o The primary glucocorticoid is secreted by adrenal cortex in response to ACTH o Binds to the hypothalamus and anterior pituitary gland to suppress CRH and ACTH in release to negative feedback loop • Aldosterone o Is a primary mineralocorticoid secreted by adrenal cortex o Once bound to receptors in kidneys distal tubes and collecting ducts, reabsorption of sodium and exertion of potassium - functions of endorphins/enkephalins and immune cytokines • Endorphins/Enkephalins o Produced in CNS and releases in response to certain stressors, by certain foods, laughter, massage/acupuncture o Reduce pain and increase euphoria and sedation • Immune cytokines o B and T lymphocytes produce several types of endorphins that are released in the response to stress - physical, behavioral, and emotional indicators of stress Physical Stress Behavioral/emotional CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Elevated BP • Increased muscle tension • Sweaty palms • Tension headache • Anxiety • Depression • Increases use of substances • Changes in eating/sleeping - explain the difference between homeostasis and allostasis • Homeostasis o The state of balance of the persons biopsychosocial systems; maintain all internal parameters to be constant • Allostasis o Refers to the overall process of adaptive change needed to maintain survival and well-being - explain what occurs during allostatic overload • When adaption mechanisms are inadequate or the total amount is excessive, overwhelming allostasis - explain why each of the following can occur due to stress: hypertension, stroke, coronary artery disease • Hypertension: can cause through repeated blood pressure elevations as well as stimulation on the NS to produce large amounts of vasoconstriction which increase blood pressure • Stroke: High levels of cortisol causes salt retention which will increase blood pressure, causing stress on blood vessels making blood clotting more likely • Coronary artery disease: high levels of cortisol from long time stress can increase blood cholesterol, blood sugar and pressure. It can promote buildup of plaque deposits in the arteries - gastrointestinal problems, immune suppression, diabetes mellitus - define glycolysis, gluconeogenesis, glycogenolysis, glycogenesis CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Protein damage: Cellular stress Excessive glycogen Variety of inorganic particles Apoptosis Cell death resulting from activation of intracellular signaling cascades. Is tidy and normally not associates with inflammation. Requires energy in cell. Cell adaptions May be due to increased functional demand or reversible cellular injury - describe and give causes and examples of each of the following cell adaptations: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, anaplasia, neoplasia Atrophy When cells reduce in size Causes: 1) disuse 2) denervation 3) ischemia 4) nutrient starvation 5) interruption of endocrine signals 6) persistent cell injury Ex: immobilization in bed rest will cause shrinkage in skeletal muscles Hypertrophy Increase in cell size Caused by increase in pathophysiological/physiological demands Ex: organ enlargement may be a result of both in hypertrophy and hyperplasia CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Hyperplasia by increasing the number of cells Cause: increased physiological demands or hormonal stimulations Ex: estrogen lease to increase in endometrial and uterine cells Metaplasia Replacement of one differentiated cell type with another. Fully reversible after injurious stimulation is removed Cause: persistent injury Ex: chronic irritation of bronchial mucosa by cigarette smoke, leads to metaplasia Dysplasia Refers to the disorganizes appearance of cells because of abnormal variations in size, shape, and arrangement. Involves complete thickness CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY of the epithelium. Can become cancerous. Anaplasia Indicated by variation in cell size within a tumor, enlarged nuclei, abnormal mitoses, and bizarre looking giant cells. Benign- slow, sometimes look like normal cells, rarely move into other organs Malignant- grow rapidly and may initiate in vessel growth Neoplasia “new growth” an abnormality of cellular growth and used interchangeably with the term tumor. - describe necrosis (all types), gangrene (all types), and apoptosis, and explain why they occur • Necrosis: Injury is too severe or prolonged to allow adaption and is usually a good consequence of disrupted blood supply o 1)coagulative, most common: manifestations of are the same regardless of the cause of death o 2) liquefaction: results from a bacterial infection that triggers a localized collection of WBC, will form a cyst, dissolution of dead cells very quickly o 3)fat: death of adipose tissue and usually results from trauma or pancreatitis o 4) caseous: lung tissue damaged by tuberculosis • Gangrene o Dry: coagulative necrosis characterized by blacked, dry, and wrinkled tissue separated by healthy tissue; normally occurs in extremities o Wet: liquefactive necrosis, found in internal organs, cold, black, may be a foul smell due to bacteria. Rapid spread can make life-threatening o Gas: formation of bubbles of gas in damaged tissue. Result of necrotic tissue by anaerobic bacteria of the genus clostridium. May be fatal. • Apoptosis: Cell death resulting from activation of intracellular signaling cascades. Is tidy and normally not associates with inflammation. Requires energy in cell. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Mutant proliferating cells begin to exhibit malignant behavior - carcinogen vs mutagen vs teratogen • Carcinogen o Applied to agents and substances capable of inducing cancer o Complete: capable of initiating genetic damage as well as promoting cellular proliferation o Partial: promoters that stimulate growth but are incapable of causing genetic mutations sufficient to initiate cancer by themselves o Ex: ultraviolet radiation, viruses, asbestos, numerous chemicals • Mutagen o A physical or chemical agent that changes genetic material, usually DNA that increases frequency of mutations • Teratogen o Environmental agents that can adversely affect the developing embryo or fetus o Includes radiation, pathogens, chemicals, and certain drugs - metastasis: define/describe, pattern of spread, tumor markers, angiogenesis, grading/staging, most common organs where metastasis occurs; what is the first place of metastasis for many cancers? • The process where cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites • For tumor cells to get access to blood circulation, they must escape, move through space, and penetrate the basement membrane of the vessel • Pattern of Spread o Survival or tumor spread is not guaranteed. It can be deterred by immune systems, destroyed, or undergo apoptosis o Some prefer specific target organs o Sometimes related to circulatory flow • Tumor Markers o Substances associated with tumor cells that may be helpful in IDing their tissue type, ID is important for prognosis and treatment o Rely on retention of some characteristics of the parent tissue type o Some released into circulation, others may have to be identified through biopsy • Angiogenesis o The process of forming new blood cells o Most tumors do not induce into late in the stage of cancer development and so remain small and vascularized for years o Begin to produce factors in response to hypoxia or other signals o Important therapeutic goal to limit tumor growth • Grading/Staging CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Done to predict tumor behavior and guide therapy o Grading- histologic characterization of tumor cells o Staging- location and pattern of tumor spread within the host • most common organs where metastasis occurs; what is the first place of metastasis for many cancers? o Liver, brain, lungs, bones o Nearby lymph nodes • - TNM system: what does each letter represent, are low or high number more severe? - generalized effects of cancer on the body System used extensively as a general framework for staging tumor - generalized effects of cancer on the body • The development of many cancers is related to lifestyle, especially tobacco and nutrition • Smoking cessation is considered important to reducing risk of cancer • Avoid excessive weight gain and alcohol intake, try to eat veggies an fruit -leukopenia vs leukocytosis, thrombocytopenia vs thrombocytosis • Leukopenia: decrease in circulating white blood cells o Malignant invasion of bone is primary cause, with malnutrition and chemotherapy as contributing factors o Major cause of morbidity in cancer patients, organism become opportunistic • Thrombocytopenia is a deficiency in the number of circulating platelets, which are important for mediating blood clots o Less than 20,000 can be associated with a spontaneous hemorrhage • thrombocytopenia: decrease in the number of platelets • thrombocytosis: increase in the number of platelets - general warning signs of cancer • Change in bowl/bladder habits • A sore that does not heal • Unusual bleeding/discharge • Thickening or lump in breast somewhere • Indigestion of difficulty swallowing • Obvious change in wart/mole • Nagging cough or hoarseness -effects of cancer therapies on the body: surgery, radiation, chemotherapy, immune therapy, gene/molecular therapy, stem cell therapy • Surgery o Majority of patients with sold tumors are treated surgically o Main benefit: removal of tumor with minor damage o Commonly accompanied with radiation therapy or chemotherapy • Radiation o Initiated apoptosis; kills tumor cell by damaging nuclear DNA CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Some normal cells killers, small does of radiation o Kills what surgery might have left over • Chemotherapy o Drug therapy, finds and kills cells, may kill some normal cells o Most effective on rapid dividing cells o Side effect: bone marrow suppression • Immunotherapy o Interferons- glycoproteins produced by immune cells in response to infection o Interleukins- peptides produced and secreted by WBC o Monoclonal antibodies- specific structures that bind to specific organs o Used with surgery, radiation and chemotherapy • Gene/Molecular Therapy o May replenish missing tumor suppression function o Genetic alteration of tumor cells to make them more susceptible to immune system; alteration of immune cells to make more efficient killers • Stem Transplant o Provides a method to restore bone marrow function after high dose radiation/therapy o Need a donor! ▪ Matched to patient: allogenic ▪ Identical twin: syngeneic ; Patients own: autologous CHAPTER 10: ALTERATIONS IN IMMUNE FUNCTION - autoimmunity: describe what is going wrong with the immune system and give examples • Immune system attacks own tissues, immune system recognizes its own cells are foreign and mounts a response that injuries self-tissues. No single theory to explain, would be multifactorial. • Cause: abnormal excessive immune responses towards own tissues • Example: in rheumatic heart disease, the body forms antibodies against the streptococcus organism and also reacts with heart valve tissue. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Chronis disease with remissions and exacerbations • Fever, joint pain, fatigue, “butterfly rash”, joint inflammation, kidney damage • Diagnosis: Difficult to diagnose as etiology is unknown, may be genetic predisposition. Combination of clinical findings and laboratory evidence. o Rash, mouth sores, arthritis, lung/heart inflammation, kidney problems, neurological, abnormal blood tests. • Organs affected: Kidney, lung/heart, neurological system • Lab results: Presence of ANA in bloodstream, lows WBC/platelets - Type IV: describe hypersensitivity problem, give examples • Delayed hypersensitivity: tissue damage resulting from a delayed cellular reaction to an antigen • Example: contact with poison ivy - what is Mantoux skin test and how does it work? how long does it take to appear? • What: confirms the diagnosis of Tuberculosis, it can only indicate if individual has had prior infection • How: PPD is injected, after 48 hours, there should be no elevation/reaction. If so, a chest X-ray is required to check for active disease. - immunodeficiency disorders: primary vs secondary, examples of each Primary Secondary Congenital, genetic, or acquired defects that directly affect immune cell function Rare, and often sex linked Predisposed to multiple deficiencies Example: Wiscott-Aldrich syndrome. Non-immune system disorders Treatments that secondarily affect immune system Excessive or defective neuroendocrine responses Excessive: increases corticosteroid increases susceptibility to infection Defective: low corticosteroid increases susceptibility to infection Factors: poor nutrition, stress, drugs, surgery Example: AIDS CHAPTER 11: MALIGNANT DISORDERS OF WHITE BLOOD CELLS - overview of WBC cancers: - leukemia vs lymphoma vs myeloma (in general) • Common neoplastic disorders of the bone marrow and lymphoid tissues • Leukemias: circulation tumors that primarily involve blood and bone marrow CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Lymphoma: tends to localize in lymph tissues; is often disseminated into other sites at diagnosis • Myeloma: malignant transformation of B-cell plasma cells; likes to form localizes tumors in bony structures - typical signs/symptoms of WBC cancer; what typically causes death to finally occur in these patients? • Malaise, weakness • Unexplained fever, night sweats • Recurrent infections • Enlarged nontender lymph nodes (lymphoma, leukemias) • Very high WBC or the presence of abnormal cell types - possible causes, common complications, main treatment methods • Possible causes: o Viruses o Radiation/chemical exposure o Reduction/alteration in normal hematopoiesis o Some genetic diseases • Common complication o Anemia: common complication of leukemia and chemotherapy o Thrombocytopenia: platelet deficiency with possible hemorrhage o Pain: common complication of both disease process and diagnostic/treatment protocols ▪ Most commonly involves bones/joints • Main Treatment Methods o Combination chemotherapy to remove malignant cells o Stem cell transplant to rescue and restore bone marrow function o Radiation and tissue-specific drug therapy may be indicated in some cases - explain why a bone marrow transplant would be needed; autologous vs allogeneic transplants • Used to manage certain leukemias. Bone marrow failure as a result of intense chemotherapy. Stem cells reintroduced into bone marrow. Close match necessary or graft- versus-host disease could occur. • Autologous: stem cells from patient’s own blood to be reinfused • Allogenic: stem cells from closely matched relatives - chronic myeloid leukemia • CML represents 15% of all cases of leukemia in the U.S - cell types affected, age at onset, clinical manifestations, prognosis (good or poor) CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Cells Affected: CML cells have greater degree of segmentation than AML cells • Age at onset: 40-50 years; occurs only occasionally in childhood/adolescence • Clinical manifestations o Characterized by malignant granulocytes that carry the Philly chromosome (Ph+) o Translocation of chromosomes 9-22 causes two genes to be juxtaposed and creates a new fusion gene: brc/abl o Symptoms: fatigue, weight loss, sweats, bleeding, abdominal discomfort (enlarged spleen) • Prognosis: o CML does not respond well to chemotherapy: poor overall survival time; if untreated average survival is 2 years o Blast stage CML (basically AML) has very poor prognosis: only 3 to 4 months CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Epstein-Barr virus Is usually present in single node or localized node chain. CHAPTER 13: ALTERATIONS IN OXYGEN TRANSPORT - functions and normal ranges for RBCs, WBCs (total, not diff. count), and platelets • RBC’s: 4.2 to 6.2 million cells; responsible for transporting oxygen and removing CO2. Important to gas transport and acid-base balance of pH. • WBC’s: 5,000 to 10,000 leukocytes/mm in blood. Protects body from phagocytosis, is a body defense mechanism. • Platelets: 150,000 to 400,000/mm3. Hemostasis after vascular injury. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - erythropoiesis: materials/substances needed, sites of production and destruction, fate of each part of hemoglobin, functions of liver, spleen, and bone marrow in this process • Definition: the production of red blood cells • Materials/substances needed: Iron, B12, Folic Acid • Sites of production/destruction: production happens in the bone marrow; destruction is by macrophages • Fate of each part of hemoglobin • Functions of liver: the primary site of synthesis • Spleen: is the primary organ to filter effete RBS out of blood • Bone marrow: produces red blood cells until a person is about 5 years old - erythropoietin: function, sites of production and action • A hormone secreted by the kidneys that increased the rate of the production of red blood cells • Sites of production: secreted mainly by the kidney in response to cellular hypoxia • Action: tissue oxygenation controls it and it controls red blood cell production, provides homeostasis in oxygen delivery to body tissues - transport of oxygen and carbon dioxide in the blood Transport of oxygen Transport of Carbon Dioxide CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Partial pressure of oxygen reflects the pressure or tension that oxygen exerts when it is dissolved in the blood- expressed as PO2; affects tendency of oxygen to bind with hemoglobin • In pulmonary capillaries, where PO2 is high, oxygen binds efficiently with hemoglobin • In the tissue capillaries, where PO2 is low, oxygen is released from hemoglobin • A shift to the left occurs in the lungs; blood is more alkalotic and carbon dioxide levels are lower- causes increased affinity of hemoglobin • A patient has fever and is acidotic, a shift to the right would cause affinity to decrease. • Transported in the blood by: dissolved gas, bicarbonate ion, and bound to hemoglobin • Partial pressure of CO2 reflects the pressure or tension it exerts when dissolved in blood- expressed as PO2 • In pulmonary capillaries, CO2 easily dissociates from hemoglobin and then diffused across the alveolar membrane into the alveolar sacs • In body tissues, CO2 inside the cells diffuses into the blood and attaches to the hemoglobin as oxygen is released to the tissues • Decreased oxygen reaching the tissues results in secretion of erythropoietin and increase RBCs • Factors like anemia or hypoxia decrease hemoglobin/atrial saturation lead to increased release of erythropoietin - function of oxygen; what is the process that produces carbon dioxide? • The function of oxygen is to make energy and make its metabolism more effective • Carbon dioxide is formed from metabolism, carbs, fats, and amino acids in a process called cellular respiration. - bicarbonate buffer system: identify each substance in the chemical equation; why is this equation important? The bicarbonate buffer system is an acid-base homeostatic mechanism involving the balance of carbonic acid (H2CO3), bicarbonate ion (HCO− 3), and carbon dioxide (CO2) in order to maintain pH in the blood and duodenum, among other tissues, to support proper metabolic function. - anemia: general description, relative vs absolute, general effects, clinical manifestations • General description o Anemia is a deficit of red cells: low oxygen-carrying capacity leads to hypoxia o Opposite of anemia: polycythemia: excess of red cells and increases blood viscosity and volume CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Renal failure Failure of the renal endocrine function impairs erythropoietin production and bone marrow compensation. Treatment Dialysis Administration of erythropoietin Decreased RBC count with low HCT and HGB level - Erythropoieti n is only used until Hgb is 12 g/dL. Replacement of iron, folate, and B12 Prognosis: 95% respond to erythropoietin therapy. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Vit B deficiency/pernicious Disruption in DNA synthesis of blast cells produces megaloblasts (macrocytic). Pernicious anemia is caused by lack of intrinsic factor leading to vitamin B12 deficiency. Folate deficiencies from dietary deficiencies, alcoholism, cirrhosis, pregnancy, or infancy - Low folate levels associated with neural tube deficits Low RBC, WBC, and platelet counts with increased MCV; megaloblastic dysplasia Peripheral nerve degeneration Megaloblastic madness Treatment For B12 administer B12 parenterally or orally and include potassium supplements. For folate, administer folic acid. Prognosis Majority respond well to treatment. Reversibility of the neurologic damage is slow. Iron deficiency Most common nutritional deficiency in the world Pica (craving for nonfood substances such as dirt, clay, ice, Treatment Oral administration CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Insufficient iron for hemoglobin synthesis Hypochromic, microcytic RBCs; low MCV, MCH, and MCHC laundry starch, cardboard, or hair) Koilonychias (spoon-shaped nails) Blue sclerae of ferrous sulfate or intravenous ferric gluconate (only in severe cases); continue for 4 to 6 months Serum ferritin level decreased; serum iron level decreased; total iron binding capacity (TIBC) increased Treat underlying cause Prognosis: Excellent Thalassemia Increased RBC destruction (hemolysis) resulting in decreased RBC survival rates Hypochromic, microcytic RBCs MCV, MCH, and MCHC are low Treatment Blood transfusions Splenectomy Associated with mutant genes that suppress the rate of globin chain synthesis Erythroblastic hyperplasia (bone marrow) Chelation therapy Bone marrow transplantation Classified by the polypeptide chain(s) with deficient synthesis Genetic counseling Prognosis: depends upon type. - α-thalassemia or β- thalassemia Most clinically severe form: thalassemia major CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Maternal antibodies cross into the fetal circulation causing destruction of fetal cells. - ABO incompatibilit y most common - Rh incompatibilit y more clinically relevant Severe cases, in utero blood transfusion and early delivery Prognosis: Death, possible retardation, or barely perceptible hemolytic process CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Absorb- take in or soak up Ccute- has relatively severe manifestations but runs short course measured in hours, days, or a few weeks. Adverse- preventing successes or development; harmful Chronic- lasts for months to years. Clinical- relating to the observation and treatment of actual patients rather than theoretical or laboratory studies Manifestations- are observed as signs of diseases, both objective and subjective Compensate-to give something in recognition of loss/injury cyanosis- a bluish discoloration of the skin resulting from poor circulation or inadequate oxygen to the blood. Cytology- the branch of biology surrounding the structure of plant and animal cells Detrimental- tending to cause harm Disseminate- spread widely Diagnosis- the identification of the nature of an illness by examination of symptoms Endemic- a disease or condition regularly found among a particular people in a certain area Epidemic- a disease is disseminated to many individuals at the same time Epidemiology- the study and analysis of the distribution and patterns of health and disease conditions in defined populations Etiology- the study of causes or reasons for a phenomena Exacerbate- to make worse Excrete- to separate and expel as waste Histology- the study of microscopic structure of tissues Hypoxemia- poor oxygenation of blood Hypoxia- a condition in which the body is deprived of adequate oxygen supply Iatrogenic- the cause is a result of an unintended or unwanted medical intervention Idiopathic- the cause is unknown Incidence- the occurrence, rate, or frequency of a crime incubation period- the interval between exposure of a tissue to an injurious agent and the first appearance of symptoms in the case of infectious diseases. Infarction- death tissue due to inadequate blood supply to the affected area Inhibit- to hold in/hold back, restrain Insidious- proceeding a gradual, subtle way, but with harmful effects Intermittent- occurring at irregular cycles Ischemia- inadequate delivery of blood to cells Latent period- the interval between exposure to a tissue to an injurious agent and the first appearance of symptoms CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Maladaptive- dysfunctional Morbidity- the condition of being diseased Mortality- the state of being subject to death Multifactorial- involving or dependent on a number of factors or causes Occlusion- the blockage or closing of a blood vessel or hollow organ Occurrence- an event/incident Pallor- an unhealthy appearance Pandemic- are epidemics that affect large regions and perhaps spreading worldwide Pathogenesis- refers to the development or evolution of a disease Pathology- the study and diagnosis of disease through examination of organs, tissues, cells, and bodily fluids Pathophysiology- the disordered physiological processes associated with disease/injury Perfusion- the passage of blood through the blood vessels or other natural channels Physiology- the branch of biology that deals with live organisms and their parts Prevalence- commonness Prodromal period- the appearance of the first signs and symptoms indicating the onset of disease Prognosis- the forecast of what is likely to come of the disease Prolonged- extend the duration of Remission- a temporary recovery Risk factor- when the link between an etiologic factor and development of disease is less than certain but the probability is increases when the factor is present Secrete- produced and discharged Sensitivity- the ability of an organism to respond to external stimuli Sequelae- a condition that is the consequence of a previous disease/injury Signs- abnormalities that signify a potential medical condition Specificity- the range of a function in which the antibody is effective Subclinical stage- during which the patient functions normally, although the disease processes are well established Symptoms- abnormalities that signify a potential medical condition Syndrome- a set of medical signs that correlate with each other and associates with a particular disease Transient- lasting only for a short time CHAPTER 2: HOMEOSTASIS AND ADAPTIVE RESPONSES TO STRESSORS CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • ACTH causes adrenal cortex to release glucocorticoids o Regulate steroid hormone cortisol by releasing it o Produced in the pituitary gland in the brain - role of posterior pituitary and function of antidiuretic hormone/vasopressin (ADH) - role of adrenal glands and functions of: • Posterior pituitary o The back portion of the master gland o Secretes oxytocin which increase uterine contractions and ADH • ADH o Increases reabsorption of water by tubules in the kidney - catecholamines – epinephrine, norepinephrine • Catecholamines o Release of is imitated through the activation of the hypothalamus gland • Epinephrine o Increases glycogenolysis (release of glucose from the liver and inhibits insulin secretion, elevating blood glucose levels) o Enhanced myocardial contractility and increases heart and cardiac output • Norepinephrine o The primary constrictor of smooth muscle in blood cells and regulate blood flow through tissues and its distribution to organs, maintaining blood pressure o Reduces gastric secretion, inhibits secretion, and innervates muscles of the eyes, dilating pupils and increasing night and far vision - corticosteroids – cortisol, aldosterone • Corticosteroids/glucocorticoids o Lipid-soluble hormones; practically every tissue in body has receptors CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Onset is slower and duration longer o Significant role in the control of the immune system • Cortisol o The primary glucocorticoid is secreted by adrenal cortex in response to ACTH o Binds to the hypothalamus and anterior pituitary gland to suppress CRH and ACTH in release to negative feedback loop • Aldosterone o Is a primary mineralocorticoid secreted by adrenal cortex o Once bound to receptors in kidneys distal tubes and collecting ducts, reabsorption of sodium and exertion of potassium - functions of endorphins/enkephalins and immune cytokines • Endorphins/Enkephalins o Produced in CNS and releases in response to certain stressors, by certain foods, laughter, massage/acupuncture o Reduce pain and increase euphoria and sedation • Immune cytokines o B and T lymphocytes produce several types of endorphins that are released in the response to stress - physical, behavioral, and emotional indicators of stress Physical Stress Behavioral/emotional CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Elevated BP • Increased muscle tension • Sweaty palms • Tension headache • Anxiety • Depression • Increases use of substances • Changes in eating/sleeping - explain the difference between homeostasis and allostasis • Homeostasis o The state of balance of the persons biopsychosocial systems; maintain all internal parameters to be constant • Allostasis o Refers to the overall process of adaptive change needed to maintain survival and well-being - explain what occurs during allostatic overload • When adaption mechanisms are inadequate or the total amount is excessive, overwhelming allostasis - explain why each of the following can occur due to stress: hypertension, stroke, coronary artery disease • Hypertension: can cause through repeated blood pressure elevations as well as stimulation on the NS to produce large amounts of vasoconstriction which increase blood pressure • Stroke: High levels of cortisol causes salt retention which will increase blood pressure, causing stress on blood vessels making blood clotting more likely • Coronary artery disease: high levels of cortisol from long time stress can increase blood cholesterol, blood sugar and pressure. It can promote buildup of plaque deposits in the arteries - gastrointestinal problems, immune suppression, diabetes mellitus - define glycolysis, gluconeogenesis, glycogenolysis, glycogenesis CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Protein damage: Cellular stress Excessive glycogen Variety of inorganic particles Apoptosis Cell death resulting from activation of intracellular signaling cascades. Is tidy and normally not associates with inflammation. Requires energy in cell. Cell adaptions May be due to increased functional demand or reversible cellular injury - describe and give causes and examples of each of the following cell adaptations: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, anaplasia, neoplasia Atrophy When cells reduce in size Causes: 1) disuse 2) denervation 3) ischemia 4) nutrient starvation 5) interruption of endocrine signals 6) persistent cell injury Ex: immobilization in bed rest will cause shrinkage in skeletal muscles Hypertrophy Increase in cell size Caused by increase in pathophysiological/physiological demands Ex: organ enlargement may be a result of both in hypertrophy and hyperplasia CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Hyperplasia by increasing the number of cells Cause: increased physiological demands or hormonal stimulations Ex: estrogen lease to increase in endometrial and uterine cells Metaplasia Replacement of one differentiated cell type with another. Fully reversible after injurious stimulation is removed Cause: persistent injury Ex: chronic irritation of bronchial mucosa by cigarette smoke, leads to metaplasia Dysplasia Refers to the disorganizes appearance of cells because of abnormal variations in size, shape, and arrangement. Involves complete thickness CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY of the epithelium. Can become cancerous. Anaplasia Indicated by variation in cell size within a tumor, enlarged nuclei, abnormal mitoses, and bizarre looking giant cells. Benign- slow, sometimes look like normal cells, rarely move into other organs Malignant- grow rapidly and may initiate in vessel growth Neoplasia “new growth” an abnormality of cellular growth and used interchangeably with the term tumor. - describe necrosis (all types), gangrene (all types), and apoptosis, and explain why they occur • Necrosis: Injury is too severe or prolonged to allow adaption and is usually a good consequence of disrupted blood supply o 1)coagulative, most common: manifestations of are the same regardless of the cause of death o 2) liquefaction: results from a bacterial infection that triggers a localized collection of WBC, will form a cyst, dissolution of dead cells very quickly o 3)fat: death of adipose tissue and usually results from trauma or pancreatitis o 4) caseous: lung tissue damaged by tuberculosis • Gangrene o Dry: coagulative necrosis characterized by blacked, dry, and wrinkled tissue separated by healthy tissue; normally occurs in extremities o Wet: liquefactive necrosis, found in internal organs, cold, black, may be a foul smell due to bacteria. Rapid spread can make life-threatening o Gas: formation of bubbles of gas in damaged tissue. Result of necrotic tissue by anaerobic bacteria of the genus clostridium. May be fatal. • Apoptosis: Cell death resulting from activation of intracellular signaling cascades. Is tidy and normally not associates with inflammation. Requires energy in cell. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Mutant proliferating cells begin to exhibit malignant behavior - carcinogen vs mutagen vs teratogen • Carcinogen o Applied to agents and substances capable of inducing cancer o Complete: capable of initiating genetic damage as well as promoting cellular proliferation o Partial: promoters that stimulate growth but are incapable of causing genetic mutations sufficient to initiate cancer by themselves o Ex: ultraviolet radiation, viruses, asbestos, numerous chemicals • Mutagen o A physical or chemical agent that changes genetic material, usually DNA that increases frequency of mutations • Teratogen o Environmental agents that can adversely affect the developing embryo or fetus o Includes radiation, pathogens, chemicals, and certain drugs - metastasis: define/describe, pattern of spread, tumor markers, angiogenesis, grading/staging, most common organs where metastasis occurs; what is the first place of metastasis for many cancers? • The process where cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites • For tumor cells to get access to blood circulation, they must escape, move through space, and penetrate the basement membrane of the vessel • Pattern of Spread o Survival or tumor spread is not guaranteed. It can be deterred by immune systems, destroyed, or undergo apoptosis o Some prefer specific target organs o Sometimes related to circulatory flow • Tumor Markers o Substances associated with tumor cells that may be helpful in IDing their tissue type, ID is important for prognosis and treatment o Rely on retention of some characteristics of the parent tissue type o Some released into circulation, others may have to be identified through biopsy • Angiogenesis o The process of forming new blood cells o Most tumors do not induce into late in the stage of cancer development and so remain small and vascularized for years o Begin to produce factors in response to hypoxia or other signals o Important therapeutic goal to limit tumor growth • Grading/Staging CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Done to predict tumor behavior and guide therapy o Grading- histologic characterization of tumor cells o Staging- location and pattern of tumor spread within the host • most common organs where metastasis occurs; what is the first place of metastasis for many cancers? o Liver, brain, lungs, bones o Nearby lymph nodes • - TNM system: what does each letter represent, are low or high number more severe? - generalized effects of cancer on the body System used extensively as a general framework for staging tumor - generalized effects of cancer on the body • The development of many cancers is related to lifestyle, especially tobacco and nutrition • Smoking cessation is considered important to reducing risk of cancer • Avoid excessive weight gain and alcohol intake, try to eat veggies an fruit -leukopenia vs leukocytosis, thrombocytopenia vs thrombocytosis • Leukopenia: decrease in circulating white blood cells o Malignant invasion of bone is primary cause, with malnutrition and chemotherapy as contributing factors o Major cause of morbidity in cancer patients, organism become opportunistic • Thrombocytopenia is a deficiency in the number of circulating platelets, which are important for mediating blood clots o Less than 20,000 can be associated with a spontaneous hemorrhage • thrombocytopenia: decrease in the number of platelets • thrombocytosis: increase in the number of platelets - general warning signs of cancer • Change in bowl/bladder habits • A sore that does not heal • Unusual bleeding/discharge • Thickening or lump in breast somewhere • Indigestion of difficulty swallowing • Obvious change in wart/mole • Nagging cough or hoarseness -effects of cancer therapies on the body: surgery, radiation, chemotherapy, immune therapy, gene/molecular therapy, stem cell therapy • Surgery o Majority of patients with sold tumors are treated surgically o Main benefit: removal of tumor with minor damage o Commonly accompanied with radiation therapy or chemotherapy • Radiation o Initiated apoptosis; kills tumor cell by damaging nuclear DNA CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Some normal cells killers, small does of radiation o Kills what surgery might have left over • Chemotherapy o Drug therapy, finds and kills cells, may kill some normal cells o Most effective on rapid dividing cells o Side effect: bone marrow suppression • Immunotherapy o Interferons- glycoproteins produced by immune cells in response to infection o Interleukins- peptides produced and secreted by WBC o Monoclonal antibodies- specific structures that bind to specific organs o Used with surgery, radiation and chemotherapy • Gene/Molecular Therapy o May replenish missing tumor suppression function o Genetic alteration of tumor cells to make them more susceptible to immune system; alteration of immune cells to make more efficient killers • Stem Transplant o Provides a method to restore bone marrow function after high dose radiation/therapy o Need a donor! ▪ Matched to patient: allogenic ▪ Identical twin: syngeneic ; Patients own: autologous CHAPTER 10: ALTERATIONS IN IMMUNE FUNCTION - autoimmunity: describe what is going wrong with the immune system and give examples • Immune system attacks own tissues, immune system recognizes its own cells are foreign and mounts a response that injuries self-tissues. No single theory to explain, would be multifactorial. • Cause: abnormal excessive immune responses towards own tissues • Example: in rheumatic heart disease, the body forms antibodies against the streptococcus organism and also reacts with heart valve tissue. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Chronis disease with remissions and exacerbations • Fever, joint pain, fatigue, “butterfly rash”, joint inflammation, kidney damage • Diagnosis: Difficult to diagnose as etiology is unknown, may be genetic predisposition. Combination of clinical findings and laboratory evidence. o Rash, mouth sores, arthritis, lung/heart inflammation, kidney problems, neurological, abnormal blood tests. • Organs affected: Kidney, lung/heart, neurological system • Lab results: Presence of ANA in bloodstream, lows WBC/platelets - Type IV: describe hypersensitivity problem, give examples • Delayed hypersensitivity: tissue damage resulting from a delayed cellular reaction to an antigen • Example: contact with poison ivy - what is Mantoux skin test and how does it work? how long does it take to appear? • What: confirms the diagnosis of Tuberculosis, it can only indicate if individual has had prior infection • How: PPD is injected, after 48 hours, there should be no elevation/reaction. If so, a chest X-ray is required to check for active disease. - immunodeficiency disorders: primary vs secondary, examples of each Primary Secondary Congenital, genetic, or acquired defects that directly affect immune cell function Rare, and often sex linked Predisposed to multiple deficiencies Example: Wiscott-Aldrich syndrome. Non-immune system disorders Treatments that secondarily affect immune system Excessive or defective neuroendocrine responses Excessive: increases corticosteroid increases susceptibility to infection Defective: low corticosteroid increases susceptibility to infection Factors: poor nutrition, stress, drugs, surgery Example: AIDS CHAPTER 11: MALIGNANT DISORDERS OF WHITE BLOOD CELLS - overview of WBC cancers: - leukemia vs lymphoma vs myeloma (in general) • Common neoplastic disorders of the bone marrow and lymphoid tissues • Leukemias: circulation tumors that primarily involve blood and bone marrow CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Lymphoma: tends to localize in lymph tissues; is often disseminated into other sites at diagnosis • Myeloma: malignant transformation of B-cell plasma cells; likes to form localizes tumors in bony structures - typical signs/symptoms of WBC cancer; what typically causes death to finally occur in these patients? • Malaise, weakness • Unexplained fever, night sweats • Recurrent infections • Enlarged nontender lymph nodes (lymphoma, leukemias) • Very high WBC or the presence of abnormal cell types - possible causes, common complications, main treatment methods • Possible causes: o Viruses o Radiation/chemical exposure o Reduction/alteration in normal hematopoiesis o Some genetic diseases • Common complication o Anemia: common complication of leukemia and chemotherapy o Thrombocytopenia: platelet deficiency with possible hemorrhage o Pain: common complication of both disease process and diagnostic/treatment protocols ▪ Most commonly involves bones/joints • Main Treatment Methods o Combination chemotherapy to remove malignant cells o Stem cell transplant to rescue and restore bone marrow function o Radiation and tissue-specific drug therapy may be indicated in some cases - explain why a bone marrow transplant would be needed; autologous vs allogeneic transplants • Used to manage certain leukemias. Bone marrow failure as a result of intense chemotherapy. Stem cells reintroduced into bone marrow. Close match necessary or graft- versus-host disease could occur. • Autologous: stem cells from patient’s own blood to be reinfused • Allogenic: stem cells from closely matched relatives - chronic myeloid leukemia • CML represents 15% of all cases of leukemia in the U.S - cell types affected, age at onset, clinical manifestations, prognosis (good or poor) CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Cells Affected: CML cells have greater degree of segmentation than AML cells • Age at onset: 40-50 years; occurs only occasionally in childhood/adolescence • Clinical manifestations o Characterized by malignant granulocytes that carry the Philly chromosome (Ph+) o Translocation of chromosomes 9-22 causes two genes to be juxtaposed and creates a new fusion gene: brc/abl o Symptoms: fatigue, weight loss, sweats, bleeding, abdominal discomfort (enlarged spleen) • Prognosis: o CML does not respond well to chemotherapy: poor overall survival time; if untreated average survival is 2 years o Blast stage CML (basically AML) has very poor prognosis: only 3 to 4 months CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Epstein-Barr virus Is usually present in single node or localized node chain. CHAPTER 13: ALTERATIONS IN OXYGEN TRANSPORT - functions and normal ranges for RBCs, WBCs (total, not diff. count), and platelets • RBC’s: 4.2 to 6.2 million cells; responsible for transporting oxygen and removing CO2. Important to gas transport and acid-base balance of pH. • WBC’s: 5,000 to 10,000 leukocytes/mm in blood. Protects body from phagocytosis, is a body defense mechanism. • Platelets: 150,000 to 400,000/mm3. Hemostasis after vascular injury. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - erythropoiesis: materials/substances needed, sites of production and destruction, fate of each part of hemoglobin, functions of liver, spleen, and bone marrow in this process • Definition: the production of red blood cells • Materials/substances needed: Iron, B12, Folic Acid • Sites of production/destruction: production happens in the bone marrow; destruction is by macrophages • Fate of each part of hemoglobin • Functions of liver: the primary site of synthesis • Spleen: is the primary organ to filter effete RBS out of blood • Bone marrow: produces red blood cells until a person is about 5 years old - erythropoietin: function, sites of production and action • A hormone secreted by the kidneys that increased the rate of the production of red blood cells • Sites of production: secreted mainly by the kidney in response to cellular hypoxia • Action: tissue oxygenation controls it and it controls red blood cell production, provides homeostasis in oxygen delivery to body tissues - transport of oxygen and carbon dioxide in the blood Transport of oxygen Transport of Carbon Dioxide CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Partial pressure of oxygen reflects the pressure or tension that oxygen exerts when it is dissolved in the blood- expressed as PO2; affects tendency of oxygen to bind with hemoglobin • In pulmonary capillaries, where PO2 is high, oxygen binds efficiently with hemoglobin • In the tissue capillaries, where PO2 is low, oxygen is released from hemoglobin • A shift to the left occurs in the lungs; blood is more alkalotic and carbon dioxide levels are lower- causes increased affinity of hemoglobin • A patient has fever and is acidotic, a shift to the right would cause affinity to decrease. • Transported in the blood by: dissolved gas, bicarbonate ion, and bound to hemoglobin • Partial pressure of CO2 reflects the pressure or tension it exerts when dissolved in blood- expressed as PO2 • In pulmonary capillaries, CO2 easily dissociates from hemoglobin and then diffused across the alveolar membrane into the alveolar sacs • In body tissues, CO2 inside the cells diffuses into the blood and attaches to the hemoglobin as oxygen is released to the tissues • Decreased oxygen reaching the tissues results in secretion of erythropoietin and increase RBCs • Factors like anemia or hypoxia decrease hemoglobin/atrial saturation lead to increased release of erythropoietin - function of oxygen; what is the process that produces carbon dioxide? • The function of oxygen is to make energy and make its metabolism more effective • Carbon dioxide is formed from metabolism, carbs, fats, and amino acids in a process called cellular respiration. - bicarbonate buffer system: identify each substance in the chemical equation; why is this equation important? The bicarbonate buffer system is an acid-base homeostatic mechanism involving the balance of carbonic acid (H2CO3), bicarbonate ion (HCO− 3), and carbon dioxide (CO2) in order to maintain pH in the blood and duodenum, among other tissues, to support proper metabolic function. - anemia: general description, relative vs absolute, general effects, clinical manifestations • General description o Anemia is a deficit of red cells: low oxygen-carrying capacity leads to hypoxia o Opposite of anemia: polycythemia: excess of red cells and increases blood viscosity and volume CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Renal failure Failure of the renal endocrine function impairs erythropoietin production and bone marrow compensation. Treatment Dialysis Administration of erythropoietin Decreased RBC count with low HCT and HGB level - Erythropoieti n is only used until Hgb is 12 g/dL. Replacement of iron, folate, and B12 Prognosis: 95% respond to erythropoietin therapy. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Vit B deficiency/pernicious Disruption in DNA synthesis of blast cells produces megaloblasts (macrocytic). Pernicious anemia is caused by lack of intrinsic factor leading to vitamin B12 deficiency. Folate deficiencies from dietary deficiencies, alcoholism, cirrhosis, pregnancy, or infancy - Low folate levels associated with neural tube deficits Low RBC, WBC, and platelet counts with increased MCV; megaloblastic dysplasia Peripheral nerve degeneration Megaloblastic madness Treatment For B12 administer B12 parenterally or orally and include potassium supplements. For folate, administer folic acid. Prognosis Majority respond well to treatment. Reversibility of the neurologic damage is slow. Iron deficiency Most common nutritional deficiency in the world Pica (craving for nonfood substances such as dirt, clay, ice, Treatment Oral administration CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Insufficient iron for hemoglobin synthesis Hypochromic, microcytic RBCs; low MCV, MCH, and MCHC laundry starch, cardboard, or hair) Koilonychias (spoon-shaped nails) Blue sclerae of ferrous sulfate or intravenous ferric gluconate (only in severe cases); continue for 4 to 6 months Serum ferritin level decreased; serum iron level decreased; total iron binding capacity (TIBC) increased Treat underlying cause Prognosis: Excellent Thalassemia Increased RBC destruction (hemolysis) resulting in decreased RBC survival rates Hypochromic, microcytic RBCs MCV, MCH, and MCHC are low Treatment Blood transfusions Splenectomy Associated with mutant genes that suppress the rate of globin chain synthesis Erythroblastic hyperplasia (bone marrow) Chelation therapy Bone marrow transplantation Classified by the polypeptide chain(s) with deficient synthesis Genetic counseling Prognosis: depends upon type. - α-thalassemia or β- thalassemia Most clinically severe form: thalassemia major CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Maternal antibodies cross into the fetal circulation causing destruction of fetal cells. - ABO incompatibilit y most common - Rh incompatibilit y more clinically relevant Severe cases, in utero blood transfusion and early delivery Prognosis: Death, possible retardation, or barely perceptible hemolytic process CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Blood loss May be from trauma or secondary to a disease process Shock and death can occur with 50% loss of circulating volume. Symptoms develop with activity at 20% loss of blood volume (tachycardia and postural drop in BP), and increase in severity with continued blood loss. Treatment: Blood volume replacement therapy with crystalloids, colloids, and fresh whole blood Prognosis: Excellent with treatment unless blood loss is severe - polycythemia: general description/definition of each type: polycythemia vera, secondary polycythemia, relative polycythemia • General Description o Excess RBCs results in increased blood viscosity, leading to clinical symptoms such as hypertension. o Types of polycythemia are categorized by a cause. • Polycythemia vera o Neoplastic transformation of bone marrow stem cells o Absolute increase in RBC mass, leukocytosis, thrombocytosis; increased uric acid because of excess proliferation; oxygen saturation normal. o Signs and symptoms from increased viscosity • Secondary Polycythemia o Caused by chronic hypoxemia with resultant increase in erythropoietin production o Increased RBC production without increase in WBCs or platelets o Identify and manage underlying cause of hypoxemia; phlebotomy may be used to decrease cardiovascular workload o Prognosis: depends on underlying condition • Relative Polycythemia o Caused by dehydration with spurious increase in RBC production o Two groups ▪ Disturbed fluid balance ▪ Stress polycythemia o Elevated hematocrit, hemoglobin, and RBC count CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 14: ALTERATIONS IN HEMOSTASIS AND BLOOD COAGULATION - hemostasis: general description, 3 parts involved in the process, triggers for intrinsic and extrinsic pathways, inadequate vs excessive • General description o Hemostasis is the arrest of bleeding or prevention of blood loss after blood vessel injury. o Involves the vessel wall, circulating platelets, and plasma coagulation proteins • Stages of Hemostasis o Primary hemostasis—initial response to vascular injury involving the interaction between platelets and the endothelium of the injured vessel ▪ Injured vessel vasoconstricts to prevent blood loss ▪ Formation of a platelet plug o Secondary hemostasis involves the formation of a fibrin clot through intrinsic and extrinsic pathways; coagulation. o Final stage: clot retraction • Triggers for intrinsic and extrinsic pathways o Intrinsic pathway is initiated when blood comes into contact with altered vascular endothelium. o Extrinsic pathway begins when the vascular wall is traumatized (crush injury). o Intrinsic and extrinsic pathways lead to the common final pathway. • Inadequate vs excessive o Hemostasis inadequate: bleeding o Hemostasis excessive: clotting/thrombosis - clotting factors: site of production, do they travel as active or inactive and why, actions of fibrinogen, prothrombin, tissue thromboplastin, calcium ions, vitamin K • Site of production: synthesized by liver • Inactive state. International standardized nomenclature. Factors are numbered in the order of their discovery, not the order in which they participate in the clotting cascade. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Ferritin- The majority of ferritin iron stores are found in the liver, spleen and bone marrow. This test is used to measure ferritin levels in the blood. Ferritin is an intracellular protein which plays a significant role in the adsorption, storage, and release of iron in the human body. • INR- A prothrombin time (PT) is a test used to help detect and diagnose a bleeding disorder or excessive clotting disorder; the international normalized ratio (INR) is calculated from a PT result and is used to monitor how well the blood- thinning medication (anticoagulant) warfarin (Coumadin®) is working to prevent blood • MCHC - The mean corpuscular hemoglobin concentration (MCHC) test is a standard part of the complete blood count (CBC) that is done during blood analysis, and the MCHC value is used to evaluate the severity and cause of anemia. • PaO2 - can be used to assess the effects of breathing problems on oxygen supply, especially in a hospital setting or during an episode of severe respiratory distress. The results are often used to determine whether emergency treatment—such as oxygen supplementation or mechanical breathing support—are needed. • CRP- C-reactive protein (CRP) is a protein made by the liver. CRP levels in the blood increase when there is a condition causing inflammation somewhere in the body. A CRP test measures the amount of CRP in the blood to detect inflammation due to acute conditions or to monitor the severity of disease in chronic conditions. • Hb- is done to check for low or high levels of red blood cells. It can be done as part of a routine checkup to screen for problems and or because a child isn't feeling well. When the level of red blood cells is low, it's called anemia. When the level is high, it's called polycythemia. • MCV- MCV blood test measures the average size of your red blood cells, also known as erythrocytes. Red blood cells move oxygen from your lungs to every cell in your body. Your cells need oxygen to grow, reproduce, and stay healthy. • Plt - is used to detect Cancer of the bone marrow or Leukaemia where cancer cells reduce the bone marrow cells, and the platelet count is drastically lowered. Renal or kidney-related diseases can also cause a reduction in platelet count. • PT- A prothrombin time (PT) is a test used to help detect and diagnose a bleeding disorder or excessive clotting disorder; the international normalized ratio (INR) is calculated from a PT result and is used to monitor how well the blood-thinning medication (anticoagulant) warfarin (Coumadin®) is working to prevent blood • TIBC- Our Total Iron Binding Capacity (TIBC) Test includes an Iron Test and is used to see if there is too much or too little iron in the blood. Iron moves through the blood attached to a protein called transferrin. • aPTT- The partial thromboplastin time (PTT; also known as activated partial thromboplastin time (aPTT)) is a screening test that helps evaluate a person's ability to appropriately form blood clots. It measures the number of seconds it takes for a clot to form in a sample of blood after substances (reagents) are added. • TST- The Mantoux tuberculin skin test (TST) is the standard method of determining whether a person is infected with Mycobacterium tuberculosis. Reliable administration and reading of the TST requires standardization of procedures, training, supervision, and practice. • RBC - A red blood cell count is a blood test that your doctor uses to find out how many CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY red blood cells (RBCs) you have. It's also known as an erythrocyte count. The test is important because RBCs contain hemoglobin, which carries oxygen to your body's tissues.....Your tissues need oxygen to function. • WBC- A white blood cell (WBC) count is a test that measures the number of white blood cells in your body. This test is often included with a complete blood count (CBC). The term “white blood cell count” is also used more generally to refer to the number of white blood cells in your body. CHAPTER 15: ALTERATIONS IN BLOOD FLOW - understand blood flow through the heart, to and from the lungs, and to and from the body: • Right atrium receives oxygen-poor blood from the body and pumps it to the right ventricle through the tricuspid valve then the • Right ventricle pumps the oxygen-poor blood to the lungs through the pulmonary valve then the • Left atrium receives oxygen-rich blood from the lungs and pumps it to the left ventricle through the mitral valve next • Left ventricle pumps the oxygen-rich blood through the aortic valve out to the rest of the body. - list, in order, all heart chambers, heart valves, and key vessels (pulmonary trunk, left and right • Chambers: Right atrium, right ventricle, left atrium, left ventricle • Valves: tricuspid valve, bicuspid or mitral valve, pulmonary semilunar valve, aortic semilunar valve • Key vessels: superior and inferior vena cava, pulmonary artery, pulmonary vein, and aorta - Vessels: a tube or canal (as an artery, vein, or lymphatic) in which a body fluid (as blood or lymph) is contained and conveyed or circulated. - which type of vessel controls BP/PR: Arteries and arterioles - and what factors influence PR? in which type does exchange of materials occur? CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - name the blood vessel that carries blood under the highest pressure: Aorta - define edema and lymphedema • Edema is the medical term for swelling. Body parts swell from injury or inflammation. It can affect a small area or the entire body. Medications, pregnancy, infections, and many other medical problems can cause edema. Edema happens when your small blood vessels leak fluid into nearby tissues. • Lymphedema - results from impairment in the circulation of lymph. - Blood vessel obstructions: - thrombus vs embolus; thrombosis/embolism in an artery or vein: clinical manifestations, effects, life- threatening locations – why would it be life-threatening? • Thrombus: a stationary blood clot formed within a vessel or a chamber of the heart o Causes: blood flow slows dramatically, becomes more turbulent, if there is damage to intimal walls or drugs o Arterial thrombosis results in ischemia o Venous thrombosis results in edema. o Inflammation in a vein: phlebitis o Inflammation with a clot in a vein: thrombophlebitis • Thrombosis o Clinical manifestations ▪ Arterial: intermittent claudication, cool, cyanotic, painful ulcer around one toe ▪ Venous: none or life threatening (pulmonary embolism), calf/groin tenderness, swelling, + Homan’s sign • Embolus o Material that forms a clot within the bloodstream; traveling clot o Embolus leaving L ventricle = ischemic stroke ▪ Differ depending on brain area affected, loss of cognitive function, CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY o Vasodilators, graft - Acute arterial occlusion: description, causes, locations where they usually occur, classic signs/symptoms • Absence of arterial circulation—emergency • May result from thrombi/emboli or mechanical compression • Classic signs and symptoms (6 Ps) o Pallor o Paresthesia o Paralysis o Pain o Polar o Pulseless - Venous flow alterations: • Incompetent valves (obesity, pregnancy, right heart failure, prolonged standing) producing varicose veins, chronic venous insufficiency, and obstruction by deep vein thrombosis • Accompanied by edema, venous stasis ulcers, and pain • Deep vein thrombosis can be life-threatening. - description and etiology of chronic venous insufficiency • Results when valvular incompetence involves the deep veins • Venous stasis ulcers are typically present, skin turns brown. • Ultrasound: best method for evaluation • Treatment: compression therapy and infection control - varicose veins: description, most common vein affected • Impaired venous return results in superficial, darkened, raised, and tortuous veins. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Greater saphenous vein most commonly affected • Treatment: increasing venous flow and reducing venous pressure; sclerotherapy and surgical interventions may be used for severe cases o Elevate legs, avoid standing, elastic stockings o Vein stripping, vein ligation - deep vein thrombosis (DVT): description, why can it be life-threatening? • Most frequently because of thrombus in a deep vein of the lower extremity • May be asymptomatic • Treated aggressively with anticoagulation therapy Previous DVT is a risk factor for further hypercoagulation. CHAPTER 16: ALTERATIONS IN BLOOD PRESSURE - Cardiac output (CO) - how is CO related to SV and heart rate (HR) – give equation: CO= HR (heart rate) * SV (stroke volume) - effects on CO when: HR increases and SV stays the same, SV decreases and HR stays the same, cardiac diseases/conditions • When HR increases and SV stays the same, CO increases • When HR stays the same but SV decreases, CO decreases - Blood pressure (BP): • Components of BP measurement o Systolic BP: peak pressure during cardiac systole o Diastolic BP: lowest pressure during cardiac diastole o SV is the primary influencing systolic pressure o SVR is the major determinant of diastolic pressure o Pulse pressure = systolic – diastolic CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - how is BP related to CO, peripheral resistance (PR), HR, and SV: BP= CO (cardiac output) * SVR (systemic vascular resistance) - effect on BP of: systemic vasoconstriction, systemic vasodilation, atherosclerosis, bradycardia and tachycardia - orthostatic hypotension • An extreme response to the change from supine to upright position; activation of the short-term control mechanisms is slow or inadequate • Causes a decrease in systolic blood pressure (>20 or >10 mm Hg within 3 minutes) when moving to an upright position • Excessive increase in heart rate (by 20 to 30 beats/min) may also be diagnostic. • Results in dizziness, blurred vision, confusion, and possible syncope • Associated with cardiovascular disease and is a risk factor for stroke, cognitive impairment, and death - hypervolemia, hypovolemia • Hypervolemia, also known as fluid overload, is the medical condition where there is too much fluid in the blood. The opposite condition is hypovolemia, which is too little fluid volume in the blood. - function of each of the following in BP regulation: sympathetic nervous system, parasympathetic nervous system, renin-angiotensin-aldosterone-system (RAAS) • Sympathetic nervous system: results in release of neurotransmitters, epinephrine and norepinephrine; short-term regulation • Parasympathetic nervous system slows heart; short term regulation • RAAS system (long-term regulation)- o Juxtaglomerular cells when stimulated by low arterial pressure release renin activates angiotensinogen to angiotensin I. o Angiotensin I when in contact with ACE activates angiotensin II, a potent vasoconstrictor and stimulates release of aldosterone. o Aldosterone, a hormone, causes reabsorption of sodium and water passively follows. o Angiotensin II produces an increase in SVR. - BP ranges for normal, pre-hypertension, and hypertension (from textbook) CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY REVIEW OF THE RESPIRATORY SYSTEM (SEE CHAPTER 21) - respiratory system overview: - structures: larynx, trachea, bronchi, bronchioles, alveoli, epiglottis, uvula • The larynx functions to prevent aspiration during swallowing and is the location of the vocal cords • The trachea, bronchi, and bronchioles serve as a conducting passageway for air, they do not engage in gas exchange • Exchange of respiratory gases occurs in the alveoli • Food is prevented from entering the trachea during swallowing by closure of the epiglottis - mechanism of normal inspiration and expiration • The process of breathing is divided into two distinct phases, inspiration (inhalation) and expiration (exhalation). During inspiration, the diaphragm contracts and pulls downward while the muscles between the ribs contract and pull upward. This increases the size of the thoracic cavity and decreases the pressure inside. As a result, air rushes in and fills the lungs. • During expiration, the diaphragm relaxes, and the volume of the thoracic cavity decreases, while the pressure within it increases. As a result, the lungs contract and air is forced out. - pulmonary volumes: tidal volume, vital capacity, residual volume • Tidal Volume: a normal breath (=500ml) or amount of gas entering and leaving lung during regular breathing • Vital capacity: total volume of gas that can be exhaled during maximal expiration (=4.8). Includes inspiratory reserve volume, and expiratory reserve volume. • Residual volume: volume of gas left in lungs at end of maximal expiration (=1.2L) CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - describe how gas exchange occurs in the lungs and at the tissues; role of CO2 in triggering breathing • Inhaled oxygen enters the lungs and reaches the alveoli. Oxygen passes quickly through this air-blood barrier into the blood in the capillaries. Similarly, carbon dioxide passes from the blood into the alveoli and is then exhaled. Oxygenated blood travels from the lungs through the pulmonary veins and into the left side of the heart, which pumps the blood to the rest of the body. Oxygen-deficient, carbon dioxide-rich blood returns to the right side of the heart through two large veins, the superior vena cava and the inferior vena cava. Then the blood is pumped through the pulmonary artery to the lungs, where it picks up oxygen and releases carbon dioxide. - explain how the lungs can control pH, including normal serum pH range, acidosis, alkalosis • The lungs control your body's pH balance by releasing carbon dioxide. Carbon dioxide is a slightly acidic compound. It's also a waste product produced by cells in the body as they use oxygen. The cells release it into your blood, and it's taken to your lungs • acidosis is caused by your lungs not being able to remove enough carbon dioxide when you exhale. This can occur when your lungs are affected by a disease or other disorder. • acidosis is a buildup of acid in the body that originates in the kidneys. It occurs when your body can’t get rid of excess acid or loses too much base. - pulmonary function tests/spirometry • Spirometry is performed by asking the patient to inhale deeply and then to exhale as quickly as possible until maximal air is exhaled. • Pulmonary function tests (PFTs) are noninvasive tests that show how well the lungs are working. The tests measure lung volume, capacity, rates of flow, and gas exchange. - importance of surfactant in fetal development • Surfactant reduces the surface tension of fluid in the lungs and helps make the small air sacs in the lungs (alveoli) more stable. This keeps them from collapsing when an individual exhale. In preparation for breathing air, fetuses begin making surfactant while still in the womb. - secondary pulmonary hypertension: description, causes, pathogenesis, clinical manifestations • It usually results from the conditions that increase the resistance of pulmonary vasculature. Disorders that reduce the total cross/sectional area of the lung increase CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY resistance and promote pulmonary hypertension. Destruction of capillaries, blockage of vessels, and vasoconstriction are examples. Tissue necrosis and hemorrhage often result. • Clinical manifestations vary according to severity and duration of pathologic process. Patients may also experience syncope, increasing dyspnea, chest pain on exertion, fatigue, hemoptysis, and edema. Eventually right sided hypertrophy will develop. - pulmonary venous thromboembolus: description, causes, clinical manifestations; why is it life-threatening? • Pulmonary emboli result in obstruction of blood flow through the part of the pulmonary system. A significant increase in pressure may result cause right sided failure. • • Emboli may be composed of fat, air, amniotic fluid, or thrombi. Thrombi is the most common cause. Generally, form in the leg under conditions of venous stasis, enhanced coagulation, or vascular trauma (Virchow’s triad). • Sudden dyspnea and chest pain, symptoms of right sided failure may be present if emboli are large. • The clot blocks the normal flow of blood. This blockage can cause serious problems, like damage to your lungs and low oxygen levels in your blood. The lack of oxygen can harm other organs in your body, too. If the clot is big or the artery is clogged by many smaller clots, a pulmonary embolism can be fatal. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY (bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and other irritating gases and particulate matter. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - description and etiology; reversible or not? explain why “blue bloater” or “pink puffer” • For patients with chronic bronchitis and emphysema, airway obstruction is persistent and irreversible. • The chronic bronchitis patient may appear as the “blue bloater”, characterizing the pathophysiologic process of oxygen desaturation (cyanosis) and edema associated with right-sided heart failure in advanced disease or exacerbations. • These patients may be referred to as “pink puffers” related to the physiologic matching of ventilation and perfusion that allows near-normal gas exchange. Ventilation–perfusion matching, and a sustained high respiratory effort produce a relatively normal arterial oxygen level until late stages of the disease. - pathogenesis, including airway changes, gas exchange, and complications/sequelae • Pathologic changes in the airway include chronic inflammation and swelling of the bronchial mucosa resulting in scarring, increased fibrosis of the mucous membrane, hyperplasia of bronchial mucous glands and goblet cells, hypertrophy of bronchial glands and goblet cells, and increased bronchial wall thickness, which potentiates obstruction to airflow. - clinical manifestations and diagnosis: radiology, pulmonary function tests, ABG, physical findings • The typical patient is an overweight man or woman (1 : 2 male-to-female ratio) in his or her 30 s or 40 s (or older) who presents with shortness of breath on exertion, excessive amounts of sputum, chronic cough, evidence of excess body fluids (edema, hypervolemia), and a history of smoking. In addition, the patient often complains of chills, malaise, muscle aches, fatigue, loss of libido, and insomnia. • In the end-stage disease process, the patient presents with signs of right-sided heart failure (distended neck veins, right ventricular heave, right ventricular gallop, and peripheral edema). Hypoxia leads to pulmonary hypertension. Cyanosis is a late sign. • Measures used to confirm the diagnosis include chest radiography, which may show increased bronchial vascular markings, congested lung fields, an enlarged horizontal cardiac silhouette, and evidence of previous pulmonary infection. • Arterial blood gas (ABG) evaluation may show elevated PaCO2 and decreased Pao2 (often below 65 mm Hg); abnormal ABGs develop early in the disease process. The electrocardiogram may reveal atrial dysrhythmias and evidence of right ventricular hypertrophy. - treatment options: medications, oxygen therapy (why?), lifestyle modifications • Pharmacologic treatment involves the use of inhaled short-acting β2 agonists and inhaled anticholinergic bronchodilators, cough suppressants, and antimicrobial agents for infections. Inhaled or oral corticosteroids may also be used in the treatment of some patients for acute exacerbations. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY • Low-dose oxygen therapy is recommended for patients with Pao2 levels less than 55 mm Hg. Mechanical ventilation may become necessary to get the patient over a crisis period of acute exacerbation • Smoking cessation is essential to decreasing the progression of the disease. A reduction i n exposure to inhaled pulmonary irritants is also advised. Supportive therapies include ad equate rest, proper hydration (8 to 12 glasses of water per day unless the patient has cong estive heart failure), and physical reconditioning programs using a treadmill or stationary bicycle. - cystic fibrosis: - description and etiology • A defect in the CFTR gene causes cystic fibrosis (CF). This gene makes a protein that controls the movement of salt and water in and out of your body's cells. In people who have CF, the gene makes a protein that doesn't work well. This causes thick, sticky mucus and very salty sweat • Cystic fibrosis is an autosomal-recessive disorder of the exocrine glands. It is the most common genetic lung disease in the United States. Cystic fibrosis can be classified either as an airflow obstructive disorder or as a suppurative (pus-forming) disorder. Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and ducts is a characteristic finding in the disease. - pathogenesis: gene involved, problem that defective gene causes, other organs/systems affected • Cystic fibrosis is classified as an autosomal-recessive disorder. More than 800 mutations in the gene that encodes for the cystic fibrosis transmembrane conductance regulator (CFTR) have been described. One genetic defect associated with cystic fibrosis involves deletion of three base pairs in codon 508 (AF508) that code for phenylalanine on chromosome 7 (band q31). This is the most common genetic mutation causing cystic fibrosis and occurs in 60% to 75% of cystic fibrosis patients tested. CFTR encodes a membrane chloride channel and is expressed in the sweat glands, the lungs, and the pancreas. Mutations in the CFTR gene result in alteration in chloride and water transport across the apical surface of epithelial cells. • Cystic fibrosis primarily affects the pancreas, intestinal tract, sweat glands, and lungs, and in males causes infertility. The mucus-producing glands in the gastrointestinal tract enlarge, generating excessive secretions.” - clinical manifestations and diagnosis: ABG, PFT, radiology, body fluids (sputum, stool, sweat), genetics CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY cyst or bleb. Tension pneumothorax is a medical emergency. that results from the buildup of air under pressure in the pleural space. Air enters the pleural space during inspiration but cannot escape during expiration. - clinical manifestations • General features include dyspnea, pleuritic pain that is sharp and worsens with inspiration, dry cough, decreased chest wall movement, absence of breath sounds, dullness to percussion, and decreased tactile fremitus over the affected area. - treatment: explain the function of inserting a chest tube • Treatment is directed at the underlying cause of the effusion and relief of symptoms. Closed chest tube drainage in adults or thoracentesis is indicated if the effusion is large. Closed chest drainage in pediatric cases is controversial. A thoracotomy to control bleeding may be required in patients with excessive bleeding (more than 200 mL/hr). - pleural effusion: • Pleural effusion, sometimes referred to as “water on the lungs,” is the build-up of excess fluid between the layers of the pleura outside the lungs. The pleura are thin membranes that line the lungs and the inside of the chest cavity and act to lubricate and facilitate breathing. - etiology, general description (including 5 major types of fluids) • The fluid has a mucoid characteristic allowing for easy movement of the lungs. The five major types of pleural effusion are: (1) transudates, (2) exudates, (3) empyema attributable to infection in the pleural space, (4) hemothorax or hemorrhagic pleural effusions, and (5) chylothorax or lymphatic pleural effusions. -clinical manifestations • Clinical features vary depending on the cause and size of the effusion. Small effusions may be asymptomatic (which is common) in patients with less than 290 mL of fluid in the pleural cavity. • General features include dyspnea, pleuritic pain that is sharp and worsens with inspiration, dry cough, decreased chest wall movement, absence of breath sounds, dullness to percussion, and decreased tactile fremitus over the affected area. -treatment • Treatment is directed at the underlying cause of the effusion and relief of symptoms. Closed chest tube drainage in adults or thoracentesis is indicated if the effusion is CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY large. Closed chest drainage in pediatric cases is controversial. A thoracotomy to control bleeding may be required in patients with excessive bleeding (more than 200 mL/hr) - pneumonia: • Refers to an inflammatory reaction in the alveoli and interstitial of the lung, usually caused by an infectious agent. - general description and high risk populations • The elderly, individuals with diminished gag reflex, hospitalized patients, hypoxic patients, and immunocompromised patients. - major causative organisms (bacteria including Mycoplasma, virus, fungus) • Pneumonia can result from three different sources: (1) aspiration of oropharyngeal secretions composed of normal bacterial flora and/or gastric contents (20% to 35% of all pneumonias); (2) inhalation of contaminants (virus, Mycoplasma); or (3) contamination from the systemic circulation. - general pathogenesis, clinical manifestations, diagnosis: radiology, sputum, bloodwork • Clinical manifestations: Clinically, the pathogenic cause, severity of the disease, and age of the patient may cause variations in the presentation of pneumonia. Some patients present with fever only. Crackles and /or bronchial breath sounds may be heard over the affected lung tissue. Patients may additionally present with chills, cough, purulent sputum, and an abnormal chest radiograph. • Diagnosis: radiology, sputum, bloodwork: Diagnosis is based on the chest radiograph, white blood cell count, and sputum culture, coupled with clinical features of fever with recurrent chills, cough, dyspnea, and rales. - pulmonary tuberculosis: - etiology: causative organism, high-risk populations, primary vs reactivating • The majority of new cases occur in malnourished individuals, those living in overcrowded conditions, immunosuppressed individuals, incarcerated persons, immigrants (36% of new cases in the United States), and elderly persons. Two-thirds of all new cases are found in racial and ethnic minorities. • TB is caused by the bacterium Mycobacterium tuberculosis, an acid-fast aerobic bacillus. Any organ system can be affected by the disease, but the most common sites are the lungs and the lymph nodes. • TB is subdivided into two major classifications: primary (usually clinically and radiographically silent) and reactivating. Primary disease (initial infection) may lie CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY dormant for many years or decades. When the person's immune system becomes impaired, reactivation may occur. HIV, corticosteroid use, silicosis, and diabetes mellitus have been found to be associated with reactivation. • Reactivation may occur many years after the primary infection. Distant organ systems may be involved as a result of hematogenous spread during the primary or reactivation phase of infection. • - pathogenesis: lung changes, lymphatic and hematogenous dissemination, granuloma and Ghon tubercle/complex formation • The pathologic manifestation of pulmonary TB is the Ghon tubercle or complex, which has parenchymal and lymph components. The parenchymal component is composed of a well-circumscribed, necrotic nodule that later becomes fibrotic and calcified. The lymph component is found in the lymph nodes. In summary, the organisms either are destroyed or persist and multiply, causing active disease. Reactivation pulmonary TB occurs months to years after the primary TB and involves apical posterior segments of the upper lobes and superior segments of the lower lobes. Mycobacterium prefer areas of high concentration of oxygen. - clinical manifestations, diagnosis: sputum, pulmonary function tests, radiology, Mantoux/PPD test • The diagnosis is made by results of sputum culture for acid-fast bacilli or by identification of the organism by DNA or RNA amplification techniques. Three consecutive morning sputum specimens are obtained to identify the slow-growing acid- fast bacillus. Chest radiographs usually show nodules with infiltrates in the lung apex and posterior segments of the upper lobes. Another diagnostic test is the tuberculin (Mantoux test) skin test (5 tuberculin units/0.1 mL of PPD injected intradermally). A second dose is administered a week later. This test does not distinguish between current disease and past infection. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY other medical problems can cause edema. Edema happens when your small blood vessels leak fluid into nearby tissues • Edema occurs when there is a decrease in plasma oncotic pressure, an increase in hydrostatic pressure, an increase in capillary permeability, or a combination of these factors. Edema also can be present when lymphatic flow is obstructed. • Decreased plasma colloid osmotic pressure results from a decreased plasma protein level, predominantly if albumin is decreased. (include hypertension, inflammation, kidney disease, liver disease, lymphatic obstruction/removal) Electrolyte Imbalances - major electrolytes found in extracellular fluid and intracellular fluid • Sodium chloride is found mostly in extracellular fluid, while potassium and phosphate are the main ions in the intracellular fluid. - sodium, potassium, calcium: hyper and hypo conditions - causes and clinical manifestations • Potassium o The normal concentration of potassium ions in plasma, is 3.5 to 5.0 mEq/L (may vary slightly with different laboratories), except in neonates, in whom it may be higher. Most of the potassium ions in the body are inside cells; the standard serum potassium measurement gives only the concentration of the small portion of potassium ions in the extracellular fluid. o Hypokalemia denotes a decreased potassium ion concentration in the extracellular fluid. The resulting clinical manifestations include abdominal distention, diminished bowel sounds, paralytic ileus, postural hypotension, skeletal muscle weakness, and flaccid paralysis. o If the serum potassium concentration rises above 5.0 mEq/L (the upper limit of normal), hyperkalemia is present. Hyperkalemia denotes an elevation of potassium ion concentration in the extracellular fluid. The main clinical manifestation at this stage is mild intestinal cramping and diarrhea, which occurs only in some individuals. • Calcium o Hypocalcemia is caused by factors that decrease calcium intake or absorption, decrease the physiologic availability of calcium, and increase calcium excretion. Clinical manifestations of hypocalcemia are those of increased neuromuscular excitability: positive Trousseau sign, positive Chvostek sign, paresthesia, muscle twitching and cramping, hyperactive reflexes, carpal spasm, pedal spasm, tetany, CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY laryngospasm, seizures, and cardiac dysrhythmias. o Hypercalcemia occurs when the serum calcium concentration rises above the upper limit of normal (11 mg/dL or 5.5 mEq/L). It indicates an elevation of the calcium concentration of the extracellular fluid. Clinical manifestations of hypercalcemia include anorexia, nausea, emesis, constipation, fatigue, polyuria, muscle weakness, diminished reflexes, headache, confusion, lethargy, personality change, and cardiac dysrhythmias. • Sodium o A normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L). Hyponatremia occurs when the sodium in your blood falls below 135 mEq/L. o Hyponatremia is a low sodium concentration in the blood. It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. Symptoms can be absent, mild or severe. Symptoms: nausea and vomiting, headache, confusion, loss of energy, drowsiness and fatigue. Also, muscle weakness, spasms or cramps. o Hypernatremia, is a high concentration of sodium in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain CHAPTER 25: ACID-BASE HOMEOSTASIS AND IMBALANCES define/describe: normal serum pH, normal serum pH range, pH values that can be fatal, acidosis and alkalosis: compensated vs uncompensated vs partially compensated • The normal pH of adult blood ranges from 7.35 to 7.45 (may vary slightly with different laboratories). The range is somewhat wider in infants and children. Table 25.1 lists normal laboratory values for pH and other acid–base parameters. If the blood and other body fluids become too acidic (reflected by pH decreased below the lower limit of the normal range), dysfunction occurs; if the pH of the blood falls below 6.9, death is likely to occur. Similarly, if the body fluids become too alkaline, as reflected by pH increased above the upper limit of the normal range, dysfunction also occurs. If the pH of the blood rises above 7.8, death is likely. CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY - normal ranges for PaCO2 and HCO3- in adults • PaCO2 normal ranges for adults are between 26-44mm Hg. HCO3- normal ranges for adults are between 22-26 mm Hg. - bicarbonate buffer system • The bicarbonate buffer system is the most important buffer in the extracellular fluid. Bicarbonate ion (HCO3−) is the base portion, and carbonic acid (H2CO3) is the weak acid portion. These two components of the bicarbonate buffer system are in chemical equilibrium in the extracellular fluid. If too much metabolic acid (e.g., lactic acid) is present, the bicarbonate ions take up hydrogen ions (H+) released by the metabolic acid and become carbonic acid. Through the action of the enzyme carbonic anhydrase, the carbonic acid then is excreted through the respiratory system in the form of carbon dioxide and water. Thus, the excess acid is neutralized when bicarbonate ions are used in the buffering process. - chemical equation, role of lungs and kidneys in regulating pH Co2 + H2O <- - -> H2CO3 <----> H+ + HCO3- - how can the lungs help to compensate for low/high pH? how can the kidneys compensate for low/high pH? • The respiratory system is the second defense against acid–base disorders. The cells continuously produce carbon dioxide (CO2). Together, CO2 and water (H2O) make carbonic acid (H2CO3). The lungs excrete carbon dioxide and water from the body. Therefore during the process of exhalation the lungs effectively excrete carbonic acid. The respiratory system adjusts the amount of carbonic acid that remains in the body by altering rate and depth of respiration. • The kidneys can excrete any acid from the body except carbonic acid (which is excreted by the lungs). These acids that are not carbonic acid are called metabolic acids because cells continuously produce them during normal metabolism. The kidneys normally excrete metabolic acids. If a metabolic acid begins to accumulate. which is more effective – the lungs or the kidneys? • Kidneys have several powerful mechanisms to control pH by the excretion of excess acid or base. - describe respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis in terms of causes, clinical manifestations, and compensatory mechanisms • metabolic acidosis CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY