PATH370 MIDTERM STUDY GUIDE INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOG, Study Guides, Projects, Research of Nursing

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PATH370 MIDTERM STUDY GUIDE WEEKS 1-2 CHAPTER 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY TERMINOLOGY Know all vocabulary and definitions from this chapter Acute: short-lived; may have severe manifestation Chronic- may last months to years, sometimes following an acute course Clinical manifestations- symptoms, signs, syndrome, latent period, prodromal period, subclinical stage, acute clinical course, chronic clinical course, exacerbation, remission, convalescence, sequelae Diagnosis- the designation as to the nature or cause of a health problem Endemic- native to a local region Epidemic- spread to many people at the same time Epidemiology- study of the patterns of disease involving populations Etiology- study of causes/reasons for phenomena Exacerbation- increase in severity, signs, or symptoms Iatrogenic- cause results from unintended or unwanted medical treatment Idiopathic- cause is unknown Incidence- reflects the number of new cases arising in a population at risk during a specified time Incubation period- the phase during which the pathogen begins active replication without producing recognizable symptoms in the host. The duration is influence by additional factors, including the general health of the host, the portal of entry, and the infectious dose Insidious- coming on gradually and subtle development PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Latent period- time between exposure of tissue to injurious agent and first appearance of signs and/or symptoms Morbidity- describes the effects an illness has on a person’s life. Not only concerned with the occurrence or incidence, but with persistence and the long term consequences Mortality- death rates for a specific population. Also described in terms of the leading causes of death according to age, sex, race, and ethnicity Multifactorial- multiple alleles at different loci affect the outcome Occurrence- frequency of a disease without defining incidence or prevalence Pandemic- spread to large geographic areas Pathogenesis- development or evolution of disease, from initial stimulus to ultimate expression of manifestations of disease Pathology- focuses on the changes in body tissues and organs that cause or are caused by disease Pathophysiology- the functional changes associated with or resulting from disease or injury Physiology- the science of the functioning of the living organism and its parts and processes Prevalence- the number of cases of a specific disease present in a given population at a certain time Prodromal period- time during which first signs and/or symptoms appear or onset of disease occurs Prognosis- the probable outcome and prospect of recovery from a disease Remission- decrease in severity, signs, or symptoms; may indicate disease is cured Risk factor- a factor that when present increases the likelihood of disease PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE reabsorption of water into the blood and to constrict blood vessels - Role of adrenal glands and functions of: ( catecholamines- epinephrine/norepinephrine, corticosteroids- cortisol/aldosterone) adrenal glands: produce hormones that help the body control blood sugar, burn protein and fat, react to stressors, and regulate blood pressure (cortisol and aldosterone) Catecholamines: enable the body to rapidly take action to fight or flee the stressor; through the sympathetic adrenal medullary system. Which releases norepinephrine and epinephrine. Catecholamines: ● Aide in elevation of cardiac output ● Vasomotor (constriction of blood vessels) changes ● Lipolysis (breakdown of fats and other lipids) ● Glycogenolysis ● Insulin suppression ● Increased respiration ● Enhanced blood coagulation Corticosteroids: they have regulatory roles in the cardiovascular system and in maintaining fluid volume, and contribute to metabolism, immunity, and inflammatory responses, brain function, and even reproduction. They are lipid- soluble hormones. ● Primary is cortisol/ aldosterone: secreted by the adrenal cortex in response to ACTH from the anterior pituitary; which is in turn affected by the release of CRH. ○ Gluconeogenisis ○ Protein catabolism ○ Inhibition of glucose uptake ○ Suppression of protein synthesis ○ Stabilization of vascular reactivity ○ Immune response suppression ( cortisol is the primary glucocorticoid. Aldosterone is the primary mineral corticoid.) - functions of endorphins/enkephalins and Immune Cytokines endorphins and enkephalins: endogenous opioids (body’s natural pain relievers) PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE +raise pain threshold; produce sedation and euphoria Cytokines are a group of proteins secreted by the immune system that act as chemical messengers. Cytokines released from one cell affect the actions of other cells by binding to receptors on their surface. You can think of these receptors as mailboxes. They receive the cytokine's chemical message, and then the receiving cell performs activities based on that message. - Physical, behavioral, and emotional indicators of stress Physical indicators: low energy, headaches, upset stomach, aches, insomnia, frequent colds Behavioral indicators: lack of punctuality, withdrawal, exhaustion, excessive behavior, unhealthy eating habits Emotional indicators: depression, moodiness, loneliness, feeling overwhelmed, isolation - Describe allostasis and explain what occurs due to allostatic overload Allostasis: addresses complexities and variable levels of activity necessary to maintain or re-establish homeostasis. The body's response to stress. The process of achieving stability through physiological or behavioral change. +carried out by a superordinate set of systems that support homeostasis in light of environmental and lifestyle changes Allostatic overload: Refers to the state in which the normal allostatic processes wear out or fail to disengage or shut off; the physiological systems are not able to adapt contributing to long term effects that can be damaging to one’s health. - Explain why each of the following can occur due to stress: hypertension, stroke, coronary artery disease, gastrointestinal problems, immune suppression, diabetes mellitus Hypertension- caused by excessive catecholamine levels and bad stress coping like smoking and bad eating habits. As well as the supply of cortisol receptors in fat cells. PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Stroke- excessive catecholamine levels and the repeated or prolonged elevation of blood pressure, especially in combination with the effects of elevated cortisol levels. Coronary artery disease- increased platelet activity, resulting in clot formation and elevated serum lipid levels. Gastrointestinal problems- the sympathetic nervous system releases norepinephrine which reduces gastrointestinal motility and gastric acid secretion. Immune suppression- chronic activation of the stress mediators produces immunosuppression and increases the risk of infection and has been implicated in the development of autoimmune diseases. Diabetes Mellitus- when cortisol levels are increased by chronic stress of either a physiological or a psychological origin, this results in obesity; which is a risk factor for decreased effectiveness of glucose transport into the cells (insulin resistance), the pathophysiologic basis for diabetes type 2. - Define glycolysis, gluconeogenesis, glycogenolysis Glycolysis: breakdown of glucose by enzymes, releasing energy and pyruvic acid Gluconeogenesis: metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates Glycogenolysis: biochemical breakdown of glycogen to glucose. Takes place in the cells of muscle and liver tissues in response to hormonal and neural signals CHAPTER 4: CELL INJURY, AGING, AND DEATH - describe and give causes and examples of each of the following cell PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Ischemia: insufficient supply of blood to an organ, usually due to a blocked artery resulting in decreased oxygen and nutrient supplies to a tissue -Can be acute, due to a sudden reduction in blood flow. Cab be chronic, due to slowly decreasing blood flow Hypoxia: derives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP in tissues -results from an inadequate amount of oxygen in the air, respiratory disease, ischemia, anemia, edema, or inability of the cells to use oxygen -occurs from severe asthma attack Hypoxemia: an abnormally low concentration of oxygen in the blood - when partial pressure of oxygen in blood is less than 60 mm Hg CHAPTER 7: NEOPLASIA - benign vs malignant tumors: terminology, appearance (gross and microscopic), growth, metastasis, necrosis, likelihood of recurrence, prognosis Malignant Tumor +can kill host if untreated +confirmed by invasive or metastasizing nature +tissue-specific differentiation (does not closely resemble tissue type of origin) -greater degree of anaplasia indicates aggressive malignancy +grows rapidly, may initiate tumor vessel growth, frequently necrotic, PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE dysfunctional +may initiate tumor vessel growth (angiogenesis) +frequently necrotic +dysfunctio nal Benign Tumor +does not have potential to kill host, but may be life-threatening because of its location +does not invade adjacent tissue or spread to distant sites +Many are encapsulated +More closely resembles original tissue type +Grows more slowly, little vascularity, rarely necrotic, often retains original function PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - abnormal behavior of malignant cells Proliferate despite lack of growth-initiating signals from the environment Escape signals to die and achieve a kind of immortality in that they are capable of unlimited replication Lose their differentiated features and contribute poorly or not at all to the function of their tissue Genetically unstable and evolve by accumulating new mutations at a much faster rate than normal cells Invade their local tissue and overrun their neighbors Perhaps worst of all: gain the ability to migrate from their site of origin to colonize distant sites where they do not belong - metastasis: define/describe, pattern of spread, tumor markers, angiogenesis, grading/staging, most common organs where metastasis occurs, first place of metastasis for many cancers Metastasis: process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites +specialized enzymes and receptors enable them to escape their tissue of origin and metastasize +specialized enzymes and receptors allow them to replicate at new site Pattern of spread +Generally spread via circulatory or lymphatic systems Tumor markers help identify parent tissue PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE +Finds cancer cell targets in the body +Most are cytotoxic +Not selective for tumor cells (normal cell death may also occur) +Most effective on rapidly dividing cells +Several courses ensure all cancer cells killed +Serious side effect: bone marrow suppression +Promising approach is to inhibit angiogenesis by the tumor with antiangiogenic drugs CHAPTER 9: INFLAMMATION AND IMMUNITY - 4 major signs/symptoms of inflammation and what causes each to occur redness- (erythema) vasodilation and increased blood flow swelling- (edema) increased capillary permeability heat- (warm to touch) vasodilation and increased blood flow pain- increased capillary permeability and irritation of nerve endings - role of chemotaxis PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE bring WBC to area - diagnostic tests indicative of inflammation leukocytosis, ^ CRP, ^ ESR, ^ plasma proteins, ^ cell enzymes, differential count - acute vs chronic inflammation; end result of chronic inflammation acute: mediators: vasodilation, increased capillary permeability, chemotaxis. Local effects: redness, heat, swelling, pain, may have exudate. Systemic effects: mild pyrexia, malaise, headache, anorexia Chronic: may develop after acute inflammation, insidious, less swelling and exudate, more lymphocytes, macrophages, and fibroblasts, more necrosis Cancer can be an end result of inflammation because inflammation relies on reactive oxygen which are secreted by neutrophils CHAPTER 10: ALTERATIONS IN IMMUNE FUNCTION Functions of all types of WBC’s: Basophils- Releases heparin to stop clotting, produce histamine to cause the blood vessels to dilate, help control inflammation, and kill parasites. Eosinophils- Kills parasites and helps control inflammation and allergic reactions Neutrophils- Removes small unwanted particles and materials from the blood Lymphocytes- Essential to the immune system and protect the body against the formation of cancer cells Monocytes- Destroys large unwanted particles in the bloodstream PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - Autoimmunity: what is going wrong with the immune system? Give examples An individual’s immune system recognizes its own cells as foreign and mounts an immune response that injures self tissues Ex. Systemic lupus erythematous, Addison disease, pernicious anemia - hypersensitivity: what is going wrong with the immune system? Normal immune response that is either: inappropriately triggered, excessive, or produces undesirable effects on the body - Type I: describe hypersensitivity problem, function/role of histamine, anaphylactic shock +Type I involves ability to respond to antigen and to produce an IgE antibody response +Released mediators cause inflammatory response +Example: allergies +Histamine: causes increased vascular permeability, vasodilation, uticaria, smooth muscle constriction, increased mucus secretion, pruritus Anaphylaxis: Life threatening because it causes systemic vasodilation combined with bronchoconstriction and edema Epinephrine needs to be administered immediately to open airways - Type II: describe hypersensitivity problem, give examples +Type II is a transfusion reaction or hemolytic disease of the newborn. The transfusion reaction is an individual that received blood from someone with a different blood group type. Hemolytic disease occurs during pregnancy PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE the Philadelphi a chromosom e (Ph+) survival time with chemotherapy, untreated has survival rate of 2 years, blast stage of CML has prognosis of 3-4 months leukemic cells with bcr/abl type to undetectable levels Allogenic BMT from suitable donor; autogenic BMT less effective Acute Lymphoblast s Peak Abrupt, bone pain, Therapy: Lymphoblast i : they look incidence: 3- 7 bruising, fever, Chemotherapy c like immature years; 2nd infection, children may for remission lymphocytes peak: middle refuse to walk, loss of induction age appetite, fatigue, abdominal pain, Post-remission enlarged spleen, liver, chemo lymph nodes with/without stem cell Prognosis: 85% 5- year transplant survival rate in indicated for children; 30% to 50% most patients in adults Monoclonal antibodies may be used in patients whose tumors express specific antigens Multipl Mature, Exclusively plasma cells 30- Antineoplas PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE e Myelo ma antibody- secr eting B in adults; usually >40 years; 95% of bone marrow, protein in urine, high serum Ca+ tic agents: induce/ maintain PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE lymphocyte s (plasma cells) median age 65 years. Men>women Onset: slow/insidio us levels, 1st symptom is bone pain, anemia, recurrent infections, bleeding tendencies, renal insufficiency, “honeycomb” appearance in ribs, spine, skull, pelvis, Bence Jones protein: malignant plasma cells produce light-chain antibody fragments that accumulate in blood and urine remission in plasma cell proliferation, high-dose chemo followed by allogenic BMT, autologous stem cell transplantatio n CHAPTER 13: ALTERATIONS IN OXYGEN TRANSPORT - functions and normal ranges for RBCs, WBCs (total, not diff. count), and platelets Total blood volume: 75.5 ml/kg in men; 66.5 ml/kg in women Blood cells make up 45% of blood volume Plasma 55% of blood volume RBC- transport oxygen to tissues, remove CO2 from tissues, buffer blood pH WBC- protect the body by phagocytosis of microorganisms, form immune antibodies Platelets- form blood clots and control bleeding, release biochemical mediator involved in the hemostatic process PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE immunologi c injury to the bone marrow stem cells symptoms include weakness, fatigue, lethargy, pallor, dyspnea, palpitations, transient murmurs and tachycardia toxic exposure Type human leukocyte antigen (HLA) and ABO to identify serologically defined loci and potential donors Pancytopenia and granulocytop eni a Maintain minimally essential levels of hemoglobin and platelets Prevent and manage infection Administer immunosuppres siv e therapy or stimulate hematopoiesis and bone marrow regeneration Vitamin B/ Inability to Premature Replacing Pernicious absorb B12, graying, slight nutritional Autoimmune , jaundice, smooth deficiencies, get gastromucos a sore beefy red B12 injections is destrpyed tongue, by antibodies paresthesias, that attack the ataxia, parietal cells, neurologic al PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE immunolog ic, surgical causes, cobalamin dietary deficiency symptoms (confusion , AMS) Iron Deficien cy Iron intake <2 mg/day (vegetarians , alcoholics), Fe malabsorpti on , Pregnancy , blood loss, RBC trauma Pallor, brittle nails, sore pale tongue, dizziness, hypoxia, pica (eat inedible thing), low ferritin Blood transfusion, Fe supplement, Vitmain C, improve diet (beef, chicken, egg yolk, turkey, whole grain) Thalassemia Sickle-Cell Africa n desce nt Blood Loss Erythrobla sti c Fetalis CHAPTER 14: ALTERATIONS IN HEMOSTASIS AND BLOOD COAGULATION - Clotting factors: site of production, effects of liver disease on clotting? Site of production- Liver PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE The liver plays a central role in the clotting process, and acute and chronic liver diseases are invariably associated with coagulation disorders due to multiple causes: decreased synthesis of clotting and inhibitor factors, decreased clearance of activated factors, quantitative and qualitative platelet defects, hyperfibrinolysis, and accelerated intravascular coagulation. - disseminated intravascular coagulation (DIC): general description, causes, why does excessive bleeding occur, lab results, treatment, is it life- threatening (why or why not)? DIC- life threatening acquired hemorrhagic syndrome in which clotting and bleeding occur simultaneously. Causes: trauma, malignancy, burns, shock, and abruption of placenta Lab results: fibrinogen level and platelet count decreased, increased bleeding time, elevated PT/INR/aPTT, elevated D-dimer/fibrin split products Treatment: removal/correction of underlying cause, support major organs, fresh frozen plasma, packed red blood cells, platelets, or cryoprecipitate, heparin used to minimize further consumption of clotting factors Lab Tests: Know what each detects. ABG- arterial blood gases, blood gas measurments are used to evaluate a person’s lung function and acid/base balance. CBC- complete blood count, test used to evaluate your overall health and detect a wide range of disorders, including anemia, infection and leukemia. CRP- C- reactive protein, blood test marker for inflammation in the body ESR- erythrocyte sedimentation rate, detects inflammation associated with conditions such an infections, cancers, and autoimmune diseases. FERRITIN- measures the amount of ferritin in a person’s blood stream. Measures iron stores in the body. Hb- detects amount of red blood cells which carry oxygen to your bodies PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - which vessel carries blood under highest pressure? in which type does exchange of materials occur? Arteries carry blood under highest pressure. Exchange of materials occurs in the capillaries. - Define edema and lymphedema Edema: swelling caused by fluid retention Lymphedema: impairment of lymphatic flow allowing fluid to collect in the interstitium - Blood vessel obstructions: - thrombus vs embolus Thrombus: stationary blood clot formed within a vessel or heart chamber. Embolus: traveling clot - Thrombosis/embolism in an artery or vein: clinical manifestations, effects, life-threatening locations – why would it be life-threatening? Thrombosis: Arterial- ischemia. Intermittent claudication, cool, cyanotic Venous- edema. None or life threatening ( pulmonary embolism) calf/groin tenderness, swelling Plebitis- inflammation in vein Thrombophlebitis- inflammation with a clot in a vein. Embolus: Embolus leaving L ventricle = ischemic stroke. PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Differs on brain area affected, loss of cognitive function, motor changer, and different levels of sensory loss. Embolus leaving R ventricle= pulmonary embolus. Acute onset of SOB, increased RR, chest pain, SUDDEN DEATH. - Arteriosclerosis/Atherosclerosis: - formation of an atheroma and major locations where they typically occur Large and medium sized arteries, Most frequently the coronary, cerebral, carotid, and femoral arteries and the aorta. - causes and risk factors including tobacco effects, complication and sequelae (Risk factors) Modifiable: -smoking -elevated BP -obesity -ineffective stress management -glucose intolerance -decreased physical activity Non-modifiable: -age -gender -ethnicity -heredity PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Hypertension is both a risk factor for the development of atherosclerosis and an outcome of it.23 Increases in both systolic and diastolic blood pressure are associated with an increased incidence of atherosclerosis. Cholesterol, the lipoproteins, and triglycerides are important in the discussion of atherosclerosis. Obesity, denied as a body weight 30% or greater than ideal, is thought to be a contributing risk factor for atherosclerosis in that it may accelerate the process - collateral circulation: the alternate circulation around a blocked artery or vein via another path, such as nearby minor vessels. - Aneurysms: - description, typical locations, diagnosis Description: localized arterial dilations, bulge outwards True aneurysms -saccular: one sided balloon -fusiform: both sides balloon out -berry: balloon has a stem/neck False aneurysms -one layer unaffected PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE HR inc. SV same: The CO is going to increase. Example can be during exercise SV dec. HR same: When the HR stays the same, cardiac output is going to decrease. Example can be an MI - Blood pressure (BP): - how is BP related to CO, systemic vascular resistance (SVR), HR, and SV BP = CO x PR (SVR), CO = HR x SV - effect on BP of: systemic vasoconstriction, systemic vasodilation, atherosclerosis, bradycardia and tachycardia, ADH and aldosterone (stress response), renin, sitting up too quickly after lying down, smoking, kidney disease vasoconstriction= high BP vasodilation= low BP atherosclerosis= high BP bradycardia= low BP, tachycardia= high BP ADH= high BP aldosterone= high BP Renin= high BP Sitting up too quickly= low BP Smoking= high PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE BP Kidney disease= high BP - function of each of the following in BP regulation: sympathetic nervous system, parasympathetic nervous system, renin-angiotensin- aldosterone-system (RAAS) SNS= increases BP PNS= decreases BP RAAS= increases BP - BP ranges for normal, pre-hypertension, and hypertension Normal= 120/80, Prehypertension= 120-139/80-89, Stage 1 hypertension= 140-159/90-99, Stage 2 hypertension= >160/>100 - How does compensation occur for changes in CO and BP? If CO decreases, HR increases and the opposite. - Primary hypertension: - description, cause, risk factors, effects of long-term/prolonged hypertension, treatment subtypes: -isolated systolic hypertension >140/<90 -isolated diastolic hypertension <140/>90 -combined systolic and diastolic hypertension: > PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE prehypertension levels Cause: idiopathic Risk factors: -Nonmodifiable: -family history -age -ethnicity/genetics -modifiable -dietary factors -sedentary lifestyle -obesity/weight gain -metabolic syndrome -high blood glucose/diabetes -high total cholesterol -alcohol and smoking -childhood and adolescent (intrauterine) -maternal smoking -pregnancy induced hypertension -dietary habits -low birth rate followed by rapid growth in both height and weight -lower socioeconomic level of mother PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE CHAPTER 18: ALTERATIONS IN CARDIAC FUNCTION - Coronary heart disease (CHD)/coronary artery disease (CAD): - description, risk factors, arterial changes insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries Risk factors: atherosclerosis, possible microcirculation abnormalities Changes: Can lead to cardiac ischemia through thrombus formation, coronary vasospasm, endothelial cell dysfunction - stable angina pectoris: description, causes, effects on the heart and if they are transitory or permanent, pattern of onset, treatment -most common -characterized by stenotic atherosclerosis coronary vessels -onset of angina pain is generally predictable and elicited by similar stimuli each time -relieved by rest and nitroglycerin - no permanent damage - myocardial infarction: -total block -chest pain (unrelieved) and radiating PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - prolonged -Irreversible - STEMI vs NSTEMI STEMI: ST elevation on ECG. patients with chest pain and evidence of acute ischemia -candidates for acute reperfusion therapy NSTEMI: patients presenting with symptoms of unstable angina and no ST elevation on the ECG -candidates for antiplatelet drugs - scar tissue formation and its effects on cardiac muscle Clinical Manifestations: -severe crushing, excruciating chest pain that may radiate to the arm, shoulder, jaw, or back -accompanied by nausea, vomiting, diaphoresis (sweating), shortness of breath -lasts more than 15 minutes and is not relieved by rest or nitroglycerin -asymptomatic MI: silent MI -Women, the elderly, and patient with diabetic neuropathies: -atypical symptoms including fatigue, nausea, PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE back pain, and abdominal discomfort -ECG changes: ST-segment elevation, large Q waves, and inverted T waves Serum marker changes -myoglobin, troponin, lactate dehydrogenase, and creatine kinase -increased CK-MB and troponin I and T - effect of MI on CO, compensatory mechanisms MI leads to drop in CO, triggering compensatory responses including sympathetic activation -SNS activation leads to increased myocardial workload by increasing: -HR -Contractility -BP - basic treatment; possible sequelae -decreasing myocardial oxygen demand -sympathetic antagonists, rest, HR control, pain relief, afterload reduction -increasing myocardial oxygen supply -thrombolysis, angioplasty, coronary bypass grafting -monitoring and managing complications PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE edema, shortness of breath) - compensatory mechanisms and explain why they eventually cause further heart damage helpful in restoring cardiac output toward normal Eventual consequences: SNS activation, increased preload, myocardial hypertrophy - left and right sided failure: - explain backward (where does blood back up) and forward (what areas are affected by impaired blood flow) effects Type Backward Effects Forward Effect Left-Sided HF Results in accumulation of blood within the pulmonary circulation, pulmonary congestion, and edema Dyspnea, dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea Cough, respiratory crackles (rales), hypoxemia, and high left-atrial pressure, cyanosis Results in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs Acute cardiogenic pulmonary edema: life threatening condition Right-Sided HF Due to congestion in the systemic venous system Edema, ascites, jugular veins distended, impaired mental Cause low output to left ventricle leading to low CO PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE functioning, hepatomegaly, splenomegaly Hepatojugular reflux test - why does biventricular heart failure occur? what further problems does this cause? Result of primary left-sided HF progressing to right- sided HF Reduced CO Pulmonary congestion due to left-sided HF Systemic venous congestion due to right- sided HF - cardiac dysrhythmias Most severe dysrhythmias and why they are life-threatening Ventricular tachycardia: three or more consecutive ventricular complexes at a rate greater than 100 beats/min, ECG depicts a series of large, wide, undulating waves, Pwaves are not associated with the QRS complexes Ventricular fibrillation: rapid, uncoordinated cardiac rhythm resulting in ventricular quivering and lack of effective contraction, ECG is rapid and erratic with no identifiable QRS complexes Atrioventricular block: problem between the sinus impulse and ventricular response -3 types: -1st degree (usually no treatment required) PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE -2nd degree (types I and II) -type I (Wenckebach, Mobitz): characterized by progressive prolongation of the PR interval until one P wave is not conducted; associated with AV nodal ischemia -type II: identified by a rhythm showing consistent PR interval with some noncunducted P waves; more serious because has a tendency to progress to complete AV (third degree) block -3rd degree (complete) -diagnosed when there is no apparent associated between atrial and ventricular conduction; is serious, as it can lead to slow ventricular rhythm and poor CO CLASSES OF MEDICATIONS FOR CARDIAC DISORDERS: On paper. CHAPTER 20: SHOCK - general description and common factor for all types of shock Common factor among all types of shock is hypoperfusion and impaired cellular oxygen utilization. This decreases CO, maldistribution of blood flow and decreased blood oxygen content Cardiogenic: inadequate cardiac output despite sufficient vascular volume, usually result of PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Structures: Larynx- A cartillaginous organ containing vocal cords for sound production. Trachea- Flexible tube of C shaped cartilage to allow air to reach lungs. Bronchi- Branches of the trachea to allow passage of air to lungs Bronchioles- Tubes connecting bronchi to alveoli. PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Alveoli- Millions of tiny sacs within the vertebrate lungs where gas exchange occurs. Simple squamous epithelium allow O2 and CO2 to diffuse into and out of the alveoli and are surrounded by blood capillaries Epiglottis- a flap of cartilage at the root of the tongue which is depressed during swallowing to cover the opening of the windpipe. Uvula- closes off the nasopharynx, preventing food from entering the nasal cavity. Mechanism of normal inspiration and expiration. During inspiration, chest wall muscles contract, elevating the ribs as the diaphragm moves downward, creating a negative intrapleural pressure. During expiration, lung deflates passively because of elastic recoil and relaxation of the diaphragm. At the end of normal expiration, alveoli still have some gas remaining, known as functional residual capacity. Surfactant decreases surface tension, allowing the alveoli to open easily with each breath. Lack of surfactant can cause the alveoli to collapse leading to atelectasis. Importance of surfactant in fetal development: Until about 36 weeks of gestational age, a fetus is in the saccular phase of lung development. During this time, surfactant production begins in the lungs. Surfactant is a soapy substance that helps keep delicate lung tissue from sticking to itself and tearing during exhalation or if the lungs are compressed. Surfactant is particularly important during delivery, as it allows the lungs to drain of amniotic fluid and fill with air properly. Premature infants are susceptible to respiratory problems and lung collapse if they are born before sufficient surfactant forms. Pulmonary volumes: Tidal volume- amount of air that moves in and out of the lungs with each breath. The normal amount of tidal volume is (500 ml.) Vital capacity- total amount of air involved with tidal volume, inspiratory reserve volume, and expiratory reserve volume. (4,500 ml) PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Residual volume- the amount of air that cannot be voluntarily expelled from the lungs. (1,500ml) Describe how gas exchange occurs in the lungs and at the tissues External respiration: During external respiration (Pulmonary gas exchange), dark red blood flowing through the pulmonary circuit is transformed into the scarlet river that is returned to the heart for distribution by systemic arteries to all body tissues. Color change is caused by O2 pick up and binding to hemoglobin in RBC, but Co2 exchange (unloading) happens equally fast. Internal respiration: Internal respiration involves capillary gas exchange in body tissues. The gas exchanges that occur between blood and alveoli and between blood and tissue cells take place by simple diffusion. Role of carbon dioxide in triggering breathing Explain how the lungs can control pH, including normal serum pH range, acidosis/alkalosis An increase in breathing rate should decrease CO2 concentration and increase oxygen concentration leading to a decrease in hydrogen ions and a pH decrease until homeostasis is met. When the CO2 reacts with water to produce carbonic acid the carbonic acid then dissociates into H+ ions and HCO3- ions. The H+ ions increase the acidity of the blood. -breath FASTER to get rid of CO2 if LOW pH -CO2 forms carbonic acid in blood -Breath SLOWER to retain CO2 if HIGH pH -CO2 combines with water to form carbonic acid in the blood Pulmonary function tests/spirometry PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE CHAPTER 22: OBSTRUCTIVE PULMONARY DISORDERS Asthma A reversible airway obstruction. Causes airway inflammation. Extrinsic- allergic, pediatric onset Intrinsic- non-allergic, adult onset Pathogenesis of allergic asthma: describe airway inflammation/cause of obstruction Exposure to a specific antigen that has previously sensitized mast cells in airway mucosa; antigen reacts with the antibody releasing chemical mediator substances. Normal respiratory epithelium replaced by goblet cells, resulting in mucosal edema, inflammatory exudates, and hyperresponsiveness of the airway. (bronchoconstriction and leakage from increased microvascular permeability) Clinical manifestations, including severe attack and status asthmaticus Wheezing, feeling of tightness of chest, dyspnea, cough (dry or productive), increased sputum production (thick, tenacious, scant, and viscid), hyperinflated chest, decreased breath sounds. Severe attack: use of accessory muscles or respiration, intercostal retractions, distant breath sounds with inspiratory wheezing, orthopnea, agitation. Diagnosis: radiology, pulmonary function test changes, abg changes Radiologic finding- hyperinflation with flattening of the diaphragm. Pulmonary function test- forced expiratory volumes decreases, peak expiratory flow rate (PEFR): determines index of airway function, ratio of PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE FEV/FVC <75% Abg- normal during mild attack. Respiratory alkalosis and hypoxemia as bronchospasm increases in intensity. PaCO2 elevation: sign that patient is getting worse. Treatment Avoid triggers: Environmental control- dust control, removal of allergens, air purifiers, air conditioners. Preventative- stop smoking, avoid second-hand smoking, aerosols, odors, early tx for respiratory infections. Medications: Bronchodilators- epinephrine (subcutaneous terbutaline, aminophylline) Intravenous corticosteroids- (mainstay of therapy) Oxygen therapy with or without mechanical ventilation. Chronic obstructive pulmonary disorder (COPD) Chronic bronchitis vs emphysema - Description and etiology; reversible or not Chronic bronchitis- Type B COPD, “blue bloater”. Hypersecretion of bronchial mucus. Chronic of recurrent productive cough >3 months. Persistent, irreversible when paired with emphysema. Emphysema- Type A COPD, “pink puffer”. Destructive changes of the aveolar walls without fibrosis. Abnormal enlargement of the distal air sacs. Damage is PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE IRREVERSIBLE. - Explain why “blue bloater” or “pink puffer” Blue bloater- excess body fluids, chronic cough, SOB on exertion, increased sputum, cyanosis (late sign). Pink puffer- use of accessory muscles to breathe, pursed lip breathing, minimal or absent cough, leaning forward to breathe, barrel chest, digital clubbing, dyspnea on exertion (late sign) Pathogenesis, including airway changes, gas exchange, and complications/sequelae Chronic bronchitis- chronic inflammation and swelling of the bronchial mucosa resulting in scarring. Increased bronchial wall thickness. Emphysema- release of proteolytic enzymes from neutrophils and macrophages leading to aveolar damage. Reduction in pulmonary capillary bed. Exchange of O2 and CO2 between alveolar and capillary blood impaired. Clinical manifestations Chronic bronchitis :overweight, SOB on exertion, excessive sputum, chronic cough (worse in the am), evidence of excessive body fluids (edema), cyanosis. Emphysema: thin, failure to thrive, use of accessory muscles, pursed lip breathing, cough, digital clubbing, barrel chest. Diagnosis Chronic bronchitis - Chest Xray - increased bronchial vascular markings, congested lung fields, enlarged horizontal cardiac silhouette. - Pulmonary function test- normal total lung capacity, increased residual volume, decreased FEV - ABG- elevated PaCO2, PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE exhale all the air from their lungs. Those with restrictive lung disease experience difficulty fully expanding their lungs. Acute/ adult respiratory distress syndrome (ARDS) - Damage to the alveolar-capillary membrane. Causes widespread protein- rich alveolar infiltrates and severe dyspnea. Occurs in association with other pathophysiological processes. - Associated with a decline in PaO2 that is refractory (does not respond) to supplemental oxygen therapy. - Causes - Severe trauma - Sepsis - Aspiration of gastric acid - Fat emboli syndrome - Shock - Flooding of the alveoli with proteinaceous fluid - Leads to the development of protein-rich pulmonary edema (noncardiogenic) - Triggers the immune system to activate the complement system and to initiate neutrophil sequestration in the lung. - Injury to pulmonary circulation - Atelectasis and decrease in lung compliance from lack of surfactant - Fibrosis of hyaline membrane - Severe Hypoxemia - Clinical Manifestations - History of precipitating event that has led to low blood volume state (shock) 1 or 2 days prior to the onset of respiratory failure - Early: sudden marked respiratory distress, slight increase in pulse rate, dyspnea, low PaO2, shallow rapid breathing - Late: tachycardia, tachypnea, hypotension, marked restlessness, frothy secretions, crackles, rhonci on auscultation, use of accessory muscles, intercoastal and sternal retractions, Cyanosis. Infant respiratory distress syndrome (IRDS) - The absence or deficiency of surfactant. - HALLMARK: hypoxemia that is refractory to increasing levels PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE of oxygen supplementation. - Decreased or altered surfactant - Atelectasis or alveolar collapse - Decrease pulmonary blood flow - Hypoventilation - Hemorrhagic pulmonary edema Clinical manifestations: - Early : shallow respirations, diminished breath sounds, intercostal/subcostal/sternal retractions, flaring of nares, hypotension, bradycardia, peripheral edema, low body temp, oliguria, tachypnea (60-120 breaths/min) - Late : frothy sputum, central Cyanosis, expiratory grunting sound, paradoxical respirations (seesaw movement of chest wall) Pneumothorax - Accumulation of air in the pleural space - Open “sucking” chest wall wound - Primary pneumothorax - Spontaneous - Occurs in tall, thin men 20 to 40 yr old - No underlying disease factors - Cigarette smoking increases risk - Secondary pneumothorax - Results of complications from pre-existing pulmonary disease - Tension pneumothorax - Traumatic origin - Results from penetrating or nonpenetrating injury - May also be from iatrogenic causes - Medical emergency - Results from buildup of air under pressure in pleural space - Air enters pleural space during inspiration but cannot escape during expiration. - Decreases venous return and cardiac output. - Clinical Manifestations - Small pneumothoraces are usually not detectable on physical exam PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - Tachycardia - Decreased or absent breath sounds on affected side - Hyperresonance - Sudden chest pain on affected side - Dyspnea - Tension and large spontaneous pneumothorax are emergency situations. - Severe tachycardia - Hypotension - Tracheal shift to contralateral (opposite) side - Neck vein distension - Subcutaneous emphysema Explain the function of inserting a chest tube A chest tube can help drain air, blood, or fluid from the space surrounding your lungs, called the pleural space. Chest tube insertion is also referred to as chest tube thoracostomy. It's typically an emergency procedure. Pleural Effusion - Pathologic collection of fluid or pus in pleural cavity as result of another disease process - Normally, 5-15 ml of serous fluid is contained in pleural space - Five major types - Transudates - Low in protein - Associated with severe heart failure or other edematous states - Exudates - High in protein - Causes: malignancies, infections, pulmonary embolism, sarcoidosis, post myocardial infarction syndrome, pancreatic disease. - Emphysema due to infection in the pleural space - High protein exudative effusion PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE Diagnosi s Treatme nt - Fever - Cough - HA - Malaise - Chest Xray shows ( parenchymal infiltrates) white shadows in involved area - Sputum C&S from deep in lungs - Bloodwork for WBC >15,000 (acute bacterial) PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - Antibiotic therapy Pulmonary Tuberculosis - is an infectious pulmonary disease caused by tubercle bacilli, bacterial airborne transmitted through droplet nuclei and emitted when coughing, sneezing, laughing, singing. - High Risk population - Prior infection - malnourishment/immunosuppression - Living in overcrowded condition - Incarcerated persons - Immigrants - Elderly - Causative organism - Mycobacterium tuberculosis - Infects lungs and lymph nodes - Infection - Inhalation of small droplets containing bacteria - Droplets expelled with cough, sneeze, talking - Primary vs Reacting - Primary (usually clinically/radiographically silent) may lie dormant for years or decades - Reacting - May occur many years after primary infection - Impaired immune system causes reactivation - HIV, corticosteroid use, silicosis, and diabetes mellitus have been found to be associated with reactivation - Pathologic manifestation is GHON tubercle or complex - Clinical Manifestations - History of contact with infected - Low grade fever - Chronic cough (most common) as disease progresses becomes productive with purulent sputum PATH370 MIDTERM STUDY GUIDE PATH370 MIDTERM STUDY GUIDE - Night sweats - Fatigue - Weight loss - Malaise - Anorexia - Apical crackles (rales) - Bronchial breath sounds over region of consolidation - Malnourished - Diagnosis - Sputum C&S (definitive diagnosis) - DNA or RNA amplification techniques (diagnosis) - PFTs - CXS - Nodules with infiltrates in apex and posterior segments - TB skin test (mantoux or PPD) - Doesn’t distinguish between current disease or past infection - False positive PPD results may occur in persons with other mycobacterial infections or if they have received bacille Calmette Guerin vaccine. - Treatment - Antibiotics CHAPTER 25: ACID-BASE HOMEOSTASIS AND IMBALANCES- OVERVIEW AND RESPIRATORY SYSTEM. - Define/ describe: normal serum pH range - Normal serum pH 7.4 - Normal pH range of adult blood 7.35-7.45 - High pH alkaline, Low pH acidic - Death can occur if pH falls below 6.9, pH rises above 7.8 - Normal ranges for PaCO2 and HCO3 in adults - PaCO2: 36-44 PATH370 MIDTERM STUDY GUIDE