NR 507 Midterm Exam 1

Afterload - The resistance to ejection of blood from the ventricle air trapping in asthma - Mast cell degranulation, triggered by the excessive amounts of IGE that have formed this individual, will bind the allergen as it enters the airway. Mast cell degranulation releases chemicals that releases mucus production and accumulation as well as chemicals that contribute to smooth muscle constriction. that smooth muscle constriction along with mucus plugs that form, result in hyperinflation of the alveoli and eventual erosion of airway tissue Anemia risk factors/causes - - Blood loss -Impaired erythrocyte production -Increased erythrocyte destruction -COmbination Aortic stenosis - - LV hypertrophy - L heart failure - Pulmonary edema - Exertional dyspnea -Syncope -Angina pectoris - Systolic murmur Asthma - - inflammation of the bronchial mucosa that causes bronchial hyperresponsiveness, bronchoconstriction, variable airflow obstruction that is reversible. -Symptoms: chest constriction, exp wheezing, dyspnea, coughing, tachycardia, tachypnea -Beta-agonist inhaler, inhaled corticosteroids, -Anticholinergic drugs:Block acetylcholine binding in the lung. Promotes bronchodilation through decrease parasympathetic response (tiotropium, ipratropium) B-thalassemia - -Greeks, Italians, and some Arabs and Sephardic Jews. -More common than A -Erythrocytes have decreased hemoglobin, and accumulations of free a chains - Mild to mod. microcytic-hypochromic anemia -slight elevation in serum iron and indirect bilirubin levels, mild splenomegaly, bronze skin, hyperplasia of bone marrow -major: severe growth delays, heart failure, liver enlargement, spinal abnormalities, lower-limb length discrepancy,facial deformity, Bronchioles - Three layer tube like structure surrounding the lumen of air passageway transition from cartilage to smooth muscle Parasympathetic stimulation releases acetylcholine for bronchial constriction= decreased airflow *dominates* Sympathetic stimulation by epi binds to b-adrendergic receptors to bronchial dilation=increased airflow Bronchitis - -Bronchial wall inflammation - Hypersecretion of mucus - Chronic productive cough (3 consecutive months for at least 2 successive years) -release of inflammatory mediators( histamine, prostaglandins, leukotrienes, interleukins) -smooth muscle constriction, hypertrophy - Airflow obstruction ( SOB, wheezing, cyanosis) - Peripheral edema - alveolar hyperinflation - CO2 retention - Irreversible Caused by: -Long-term exposure to environmental irritants - Repeated episodes of acute bronchitis - Factor(s) affecting gestational or childhood lung development - the most common being pre-term birth and/or RSV infection in early infancy calcium binding and troponin - In resting muscle the myosin-binding sites are covered by troponin and tropomyosin. The calcium ions released into the sarcoplasm as a result of the action potential bind to the troponin. This binding causes the tropomyosin and troponin to move out of the way of the myosin-binding sites, leaving the myosin heads free to bind to the actin microfilament. Cardiac output - HR x SV -Normal= 5Lpm -Preload, afterload, contractility, heart rate Causes of renal failure - - AKI - HTN -DM -Lupus Collecting duct - Reabsorption of H2o (ADH required) reabsorb or secret Na, K, H, Nh3 Urea reabsorbed in medulla Final concentration