NR507 Advanced Pathophysiology Week 4 Midterm Exam with 100% Verified Solutions, Study Guides, Projects, Research of Nursing

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NR507 Advanced Pathophysiology Week 4 Midterm Exam with 100% Verified Solutions Hypersensitivity: Type 1 -Mediated IgE -inflammation due to mast cell degranulation -anaphylactic, asthma, hay fever treatment: epinephrine Hypersensitivity: Type 2 -Cytotoxic reaction: tissue specific -binds to the antigen ON THE CELL SURFACE -macrophages are primary effectors cells involved cause tissue damage or alter function Hypersensitivity 2 -Graves’ Disease (hyperthyroidism) -alters function not destroy -blood transfusions reaction- transfused erythrocytes are destroyed by agglutination or lysis -drug allergies -hemolytic anemia Hypersensitivity: type 3 -Not organ specific -antibody binds to soluble antigen OUTSIDE THE CELL SURFACE that was released into the blood or bodily fluids, and the complex is then deposited in the tissues Hypersensitivity: Type 3 -rheumatoid arthritis -Systemic Lupus Erythematosus (SLE) -Raynaud's Hives (urticaria) Hypersensitivity Type 1 First responders to innate the immune system Neutrophils Allergic contact dermatitis Hypersensitivity Type IV Type 2 cytotoxic hypersensitivity mediated by: -IgG IgM -macrophages are primary effort cells - Serum Sickness type 3 hypersensitivity Hypersensitivity IV, -is more of a delayed immune response. -mediated T-cells attack tissue directly (no antibodies) Autoimmune -diseases in which the body makes antibodies directed against its own tissues - Primary immunodeficiency Normal hemoglobin for women RBC The number of erythrocytes in 1 cubic mm of whole blood Hemoglobin (Hgb) The oxygen-carrying pigment of red cells Hematocrit (Hct) The volume of cells as a % of total volume of cells and plasma in whole blood 42-45% Normal for HCT for men 37-48% Normal HCT for women Mean Cell Volume (MCV) Measures the average size of the RBC 80-100 fL Normal MCV RDW (red cell distribution width) Estimate of the uniformity of individual cell size 11.5- 14.5% Normal RDW Microcytic (MVC <80fL) Iron deficiency Microcytic (MVC <80fL) less than Sideroblastic Microcytic (MVC <80fL) Thalassemia Microcytic (MVC <80fL) Anemia of chronic disease Normocytic (MVC 80-99) Anemia of inflammation and chronic disease Normocytic (MVC 80-99) Hereditary spherocytosis Normocytic (MVC 80-99) G6PD deficiency Normocytic (MVC 80-99) Paroxysmal nocturnal hemglobinuria Macrocytic (MVC >100) greater than B12 deficiency (pernicious anemia) Macrocytic (MVC >100) greater than Folate deficiency Hypochromic anemia -(MCHC) less than normal hemoglobin RBCs pale in color Normochromic anemia -(MCHC) normal hemoglobin Neither pale or dark Hyperchromic anemia - (MCHC) more than normal hemoglobin Dark rue or red Manifestations of anemia fatigue, pallor, weakness, dyspnea, dizziness, tachycardia iron deficiency anemia -microcytic, hypochromic -can cause excessive bleeding -treatment: iron supplements -insufficient iron levels or the inability of the cells mitochondria to utilize iron effectively Ferritin Measurement that reflects the body's total iron stores microcytic hypochromic anemia -iron deficiency anemia -sideroblastic -thalassemia Microcytic Normochromic Anemia of inflammation and chronic disease Microcytic Hyperchromic Hereditary spherocytosis Lack of intrinsic factor causes pernicious anemia Folic acid is essential for the body because It plays a role in maturing of RBCs Liver disease causes Non-megaloblastic anemia Macrocytic Anemia's -antibiotics and other meds: PCN, phenytoin, diuretics, anti diabetic, sulfa -congenital defects: fanconi's anemia ___ used to diagnose aplastic anemia -Blood test and bone marrow biopsy -granulocyte count less than 500 -platelet count less than 20,000 -absolute reticulocyte count less than or equal to 40x 109/L Post hemorrhage: lab Reticulocyte count is high MCHC normal sickle cell anemia -a genetic disorder that causes abnormal hemoglobin, resulting in some red blood cells assuming an abnormal sickle shape sickle cell anemia -autosomal recessive gene disorder -two abnormal genes, one form each parent Patho of sickle cell -Involves a single amino-acid change on the beta-chain -4 genes involved in encoding synthesis of the alpha protein chains for Hb. Genes located on chromosome 16 Hemoglobinopathies sickle cell and thalassemia Thalassemia -Autosomal recessive genetic disorder -abnormal Hb gene from each parent like sickle cell -many possible genetic mutations -single or muitlple amino changes on alpha and beta chains Manifestations of Sickle cell -Involves single Amino acid change on the betachai -Increased RBC hemoglobin S concentration, dehydration, acidosis, hypoxemia -have a cute painful episodes Manifestation of thalassemia -May have possible genetic mutations - ineffective erythropoiesis -occurs and people from south east Asia and China Patho of heart failure *less cardiac output -Heart tries to compensate for not pumping an adequate amt of blood -Increased heart rate -Blood vessels dilate -Heart hypertrophy -Right side triggered by MI or lung dx -Vascular resistance -Greater O2 demand -Cells become hypoxic Heart failure overtime causes....resulting in increase preload -decreased contractility -decreased stoke volume -increase left ventricular end-diastolic volume (LVEDV) Long-standing cause of heart failure Hypertension Flow of the heart: Inferior/Superior vena cava, right atrium, tricuspid valve, right ventricle, pulmonary semi lunar valve, pulmonary arteries, (deox), lungs, pulmonary veins, left atrium, mitral valve, left ventricle, aortic semi lunar valve, aorta, (oxy) Flow of the heart a. Right Atrium, Right Ventricle, Pulmonary Arteries, Lungs, Pulmonary Veins, Left Atrium, Left Ventricle, Aorta right sided heart failure manifestations 1. Jungular Vein Distention 2. Ascending Dependent Edema 3. Weight Gain 4. Hepatomegaly (Liver Enlargement 5. cor pulmonale right sided heart failure Right sided heart failure can occur due to left sided heart failure due to the back up of the fluid from the left side of the heart Preload Patient at risk for heart failure who have not yet developed structural heart changes (those with diabetes, those with coronary disease without prior infarct) Stage B HF Patients with structural heart disease reduce ejection fraction (left ventricular hypertrophy chamber enlargement) who have not yet developed symptoms of heart failure -structural heart damage, but no damage Stage C HF Patients you have developed clinical heart failure -symptomatic Stage D HF Patients with refractory heart failure that require advance intervention -example the need for bio -ventricular pacemaker left ventricular assist device or a heart transplant Class I HF No limitation of physical activity Class II HF -Slight limitation of physical activity -Patient is comfortable at rest but ordinary physical activity results and symptoms of HF Class 111 HF -There is marked limitation of physical activity -the patient is comfortable at rest but less than ordinary activity causes symptoms of HF Class IV HF The patient is unable to carry on any physical activity without symptoms of HF or they have symptoms of HF at rest Transition of stages of HF: -Once a stage has been reached the person can ever go back to the prior stage -the damage of the heart cannot be reversed Transition of classes in HF The patient may move between classes one and four as symptoms can be improved through treatment wand medications Manifestations of Right HF -Jugular vein distention -heptatosplenomegal -peripheral Edema -cor pulmonale tricuspid valve damage Left HF manifestations -Increase left ventricular afterload -decrease ejection fraction -increased left ventricular preload -pulmonary edema -Dyspnea CAD Long-standing atherosclerosis aortic stenosis murmur Mid-systolic crescendo-decrescendo heard loudest at the base and radiating to the neck Aortic regurgitation murmur -Diastolic rumbling murmur heard at the apex of the heart -An early high-pitched diastolic murmur hired at the left lower sternal border -A systolic crescendo-descrescendo murmur heard at the left upper sternal border Mitral Stenosis murmur Low pitch murmur auscultated at the hearts Apex Mitral regurgitation murmur Pansystolic, often loud, blowing, best heard at apex, radiates well to left axilla aortic stenosis -calcification of aortic valve cusps that restricts forward flow of blood during systole -narrowing of the aorta -S4 gallop -fainting, chest pressure -left ventricular hypertrophy mitral regurgitation -Reflux of blood from left ventricle into left atrium during systole -dyspnea, Jugular vein distention aortic regurgitation -flow of blood backward from the aorta into the heart; caused by a weak heart valve -severe SOB chest x-ray shows signs of pulmonary edema and cardiomegaly mitral stenosis Determining the severity: mild >70% Determining the severity: moderate 60-70% Determining the severity: Moderately Severe 50-60% Determining the severity: severe 35-50% Determining the severity: Very severe <35% Causes air trap in the Longs after full expirationobstructive disorders definition COPD and asthma -Characterized by extraction of airflow during expiration -Shortness of breath when exhaling air -Causes air trap in the Longs after full expiration Types of COPD: irreversible chronic bronchitis and emphysema Restrictive disorders definition -Characterized by reduction in lung volume -Results in difficulty in taking air into the lungs -Due to stiffness and lung compliance or chest wall structural abnormalities -Includes interstitial lung disease, sclerosis, neuromuscular causes and significant obesity Chronic bronchitis will decrease ? FEV1 Emphysema has a late effect of__? Hypoxia and hypercapnia A patient with chronic bronchitis is likely to experience__? Respiratory acidosis due to inability to exhale CO2 Presentation of COPD on X-ray A flatten diaphragm, distended lung fields, and increased thoracic diameter GOLD criteria for COPD: stage 1: mild FEV1 % predicted 80-100% GOLD criteria for COPD: stage 2: moderate FEV1 % predicted 50%-80% GOLD criteria for COPD: stage 3: severe FEV1 % predicted 30-50% GOLD criteria for COPD: stage 4: very severe FEV1 % predicted Less than 30% Emphysema -hyperinflation of air sacs with destruction of alveolar walls (damage occurs in the airway, but the aveloi -air trapping -purses lip breathing -barrel chest Chronic Bronchitis definition -Bronchial inflammation hypersecretion of mucus and chronic productive cough that persist for at least three consecutive months for at least two successful years Result of chronic bronchitis -Excessive mucus production accumulation -hypertrophy of bronchial smooth muscles - hypertrophy and hyperplasia of chronic bronchial mucus producing cells -airflow obstruction -and decreased alveolar ventilation -(irreversible) Manifestations of chronic bronchitis -Productive and purulent cough -copious sputum production -Dyspnea - wheezing -rhonchi -cyanosis of the skin and mucous membranes -and peripheral edema Patho of chronic bronchitis Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall. chronic low oxygen -The kidneys compensate by increasing secretion of a erythropoietin the primary hormone results for simulating red blood cell production