NR 507 Pulmonary Latest 2024 100% Pass

NR 507 Pulmonary Latest 2024 100% Pass Anticholinergic drugs for asthma Fast-acting treatment for asthma -Tiopropium and Iprapropium -block acetylcholine binding (remember this is NT transmitter released in the parasympathetic stimulation which causes constriction of the bronchi by blocking it, we decrease the parasympathetic response therefore preventing constriction. -Atrovent & Spiriva both prevent the muscle bands around the airways from tightening thus reduce in exacerbation. Asthma A chronic allergic disorder characterized by episodes of severe breathing difficulty, coughing, and wheezing. -Characterized by: 1. Airway inflammation 2. Bronchial hyperactivity 3. Intermittent, reversible airflow obstruction. causes of asthma complex interaction of genetic and environmental factors Results in: 1. Excess mucus production/accumulation 2. Hypertrophy of smooth muscle 3. Airflow obstruction 4. Decreased alveolar ventilation. extrinsic asthma triggered by a chronic allergic reaction eg - mold, pollen, dust mites, pet dander -elevated IgE level is diagnostic -more common, especially in children (males:females = 2:1) S/S Coughing, wheezing, SOB, tachypnea, chest tightness. Intrinsic asthma -triggered by a variety of non-allergic factors eg - chemicals, air-borne irritants, infections (esp. viral), exercise, stress, anxiety, GERD, obesity -no initial elevation in IgE level -typically seen in adults (<40 y/o) (slightly more common in females) patho of asthma 1.Allergen enters body 2. Ag binds, mast cells (which have IgE) degranulate (histamine, prostaglandins, leukotrienes, interleukin) 3. Leads to smooth muscle constriction > mucus secretion > vasodilation >edema > more WBC to site (too many) dendritic cells, T H 2 cells (T helper 2) > Stimulate B-cells > More IgE > Eosinophils and neutrophils to site >Inflammation > Leads to damage of tissue > which can further lead to permanent airway remodeling (resulting in extrinsic asthma). Alveolar Hyperinflation in Asthma Plugs of mucus and pus, caused by the process explained above, from the inflammatory process can block alveolar passageways, leading to air-trapping inside the alveoli, causing hyperinflation. > This can also occur with bronchitis. short acting beta 2 agonists Fast-acting treatment for asthma -Albuterol, Levalbuterol (Xopenex) and Pirbuterol (Maxamir) -Activate Beta receptors (remember the sympathetic stimulation which causes dilation of the bronchi). Albuterol increases the sympathetic response. oral corticosteroids Fast-acting treatment for asthma -prednisone, methylprednisolone -help reduce inflammatory response by inhibiting inflammatory cell response and chemical production. long acting: Inhaled Corticosteroids -inhibit inflammatory cell and chemical production that reduce inflammatory process Examples: beclomethasone, triamcinolone, Ciclesonide (Alvesco) Fluticasone (Flovent HFA) Mometasone (Asmanex Twisthaler, Asmanex HFA)corticosteroid Mast Cell Stabilizers -prevent release of inflammatory chemicals reduce inflammatory process by ↓ degranulation -remember degranulation of mast cells causes the inflammatory response by release of histamine, prostaglandins, leukotrienes, interleukin EX: Cromolyn Leukotriene Modifiers -leukotrienes are released from mast cell degranulation and cause inflammation. This drugs block leukotriene synthesis and/or interaction reducing the inflammatory process. Ex: Montelukast (Singulair) long acting beta 2 agonists (LABA) -activate beta receptors (primarily in lung) bronchodilation through ↑ sympathetic response Ex: Salmeterol Methilxanthines -inhibits enzymes to allow for smooth muscle relaxation > bronchodilation Ex: theophylline Monoclonal antibodies -block ability of IgE to trigger degranulation of mast cells therefore reducing inflammatory process (remember IgE is produced in excess, especially in extrinsic asthma). Ex: Omalizumab acute bronchitis -infection and inflammation of bronchial tubes (bronchi) chronic bronchitis -inflammation of the bronchi persisting over a long time -Chronic productive cough (which persists at least 3 consecutive months, for at least 2 years) Caused by: 1. Long-term exposure to environmental irritants 2. Repeated episodes of acute bronchitis ( (infection) 3. Factors affecting gestational or childhood long development (pre- term birth, infancy RSV) -Lung damage is irreversible patho of chronic bronchitis -Exposure to airborne irritants (most common tobacco, others air pollution, . industrial chemicals) > exposure leads to smooth muscle constriction (remember parasympathetic response to protect us) > - -Mucus secretion follows > Release of inflammatory mediators (similar to asthma - histamine, prostaglandins, leukotrienes, interleukin- this happens in the middle layer of the bronchioles - remember the lamina propia). This process is normal and expected, now What happens with long-term exposure to these irritants symptoms of chronic bronchitis -Productive/purulent cough -copious sputum production, wheezing or rhonchi (fluid/mucus movement in the airway) -cyanosis (bluish discoloration of skin and mucus membranes indicating poor tissue oxygenation), SOB, peripheral edema. All these symptoms indicate a decreased ability of lungs to ventilate and perfuse. polycythemia vera -condition characterized by too many erythrocytes; blood becomes too thick to flow easily through blood vessels. -chronic neoplastic, nonmalignant condition characterized by over production of red blood cells and splenomegaly -Symptoms: headache, erythromelalgia, pruritis (especially to hot water) Acid/ base disturbance- COPD -chronic obstructive pulmonary disorder. Causes air trapping. Increasing CO2 retention and respiratory acidosis. Perfusion -The passage of fluid to an organ or a tissue, usually referring to the delivery of blood to an area. Blood flow of heart Enters the right side inferior/superior vena cava- emptying deoxygenated blood to right atrium- right ventricle, through tricuspid valve, pulmonary valve, pulmonary artery to lungs (where it is oxygenated). Pulmonary vein empties oxygen rich blood to left atrium/ left ventricle, through mitral valve, aortic valve, aorta---->to the body. bronchioles function passage of air to alveoli- gas exchange