NR-507 Mid-Term Study Guide

NR-507 Mid-Term Study Guide Hello Class, This study guide is for the 50 question multiple choice Mid-Term exam that will be given during Week 4. It will cover the following concepts: Pulmonary: review concepts related to anticholinergic drugs and the treatment for asthma, bronchitis and associated pathogenesis; We are now ready to address the pathogenesis of chronic bronchitis which begins with some sort of exposure to airborne irritants which activates bronchial smooth muscle constriction, mucus secretion, and release of inflammatory mediators (histamine, prostaglandins, leukotrienes, interleukins) from immune cells located in the lamina propria These airborne irritants can include air pollution or industrial chemicals & fumes. But the most common irritant is smoke from cigarettes and other tobacco products. Keep in mind that all of these bronchial responses are, in fact, normal responses to occasional inhalation of airborne irritants. Smooth muscle constriction is important to limit passage of the irritant deeper into the respiratory tract. Secretion of mucus and release of inflammatory chemicals are also important to help trap and defend against a potential harmful substance. The transition from a normal, protective respiratory response to a detrimental effect occurs with …. long-term exposure to airborne irritants which promotes  smooth muscle hypertrophy à increased bronchoconstriction  hypertrophy and hyperplasia of goblet cells à mucus hypersecretion  epithelial cell metaplasia à non-ciliated squamous cells  migration of more WBCs to site à inflammation & fibrosis in bronchial wall  thickening and rigidity of bronchial basement membrane à narrowing of bronchial passageways chronic bronchitis and related acid/base disturbances, Because of the anatomical changes in the bronchioles associated with chronic irritation ventilation, especially exhalation, is compromised. Pressure differences during inhalation are high enough to force air into the alveoli. However, during exhalation the narrowing and collapse of the air passageways causes air to be trapped in the alveoli resulting in.  alveolar hyperinflation à expanded thorax  hypercapnia (CO2 retention) à respiratory acidosis What is chronic bronchitis? This is a chronic disease characterized by: bronchial inflammation, hypersecretion of mucus, and chronic productive cough, persisting for at least 3 consecutive months for at least 2 successive years Chronic bronchitis is caused by: long-term exposure to environmental irritants, repeated episodes of acute bronchitis (infection), and factor(s) affecting gestational or childhood lung development – the most common being pre-term birth and/or RSV infection in early infancy Chronic bronchitis results in: excess mucus production and accumulation, hypertrophy of bronchial smooth muscle, hypertrophy & hyperplasia of bronchial mucus-producing cells, airflow obstruction, and decreased alveolar ventilation The lung damage from chronic bronchitis is typically considered irreversible. The most common symptoms of chronic bronchitis are:  productive, purulent cough  copious sputum production  shortness of breath  wheezing, rhonchi – sounds typically associated with fluid/mucus in the airways  cyanosis – bluish discoloration of the skin and mucous membranes associated with poor oxygenation  peripheral edema perfusion, he high concentration of CO2 creates unfavorable conditions for gas exchange, so there is  decreased O2 exchange à ventilation/perfusion (V/Q) mismatch Decreased perfusion of the pulmonary capillaries with oxygenated blood results in  chronic pulmonary hypoxia à cyanosis (the term “blue bloater” used to describe a client with chronic bronchitis, with bloater referring to the expanded thorax that these individuals can develop as a result of alveolar hyperinflation) Poor ventilation, leading to decreased perfusion, causes Right to Left “shunting” to occur. This is the phenomenon where deoxygenated blood passes from the RV to lungs to the LV without adequate perfusion (gas exchange) Perfusion, the actual exchange of O2 and CO2 in the bloodstream, occurs via the alveoli and pulmonary capillaries. Ventilation, air movement in/out of the lung, is critical to ensure sufficient perfusion. blood flow between the heart and lungs, Blood enters the heart through two large veins, the inferior and superior vena cava, emptying oxygen-poor blood from the body into the right atrium. ... As the ventricle contracts, blood leaves theheart through the pulmonic valve, into the pulmonary artery and to the lungs where it is oxygenated.Feb 4, 2019 asthma signs and symptoms, The most common symptoms of both extrinsic and intrinsic asthma are: coughing, wheezing shortness of breath rapid breathing chest tightness, difficulty breathing/ bronchioles, After air enters the nasal and/or oropharynx it passes into the trachea which branches into Left & Right bronchi, which further divide into smaller passageways called the bronchioles, and finally almost 30 branch points later, form the actual gas exchange areas called the alveoli The bronchioles or bronchioli are the smaller branches of the bronchial passageways in the respiratory tract that deliver air to the smaller terminal bronchioles in the conducting zone, and even smaller respiratory bronchioles in the respiratory zone. The bronchioles no longer contain the cartilage, that is found in the bronchi, or glands in their submucosa. To understand the pathophysiology of asthma we need to look a little more closely at the structure of the airways, especially in the bronchioles. The bronchioles are a three layer tube like structure surrounding the lumen or air passageway. The innermost layer, closest to the lumen, is composed of columnar epithelial cells and mucus producing goblet cells. The outermost layer is composed of smooth muscle cells, responsible for the ability of the airways to constrict and dilate. The middle layer, called the lamina propria, is embedded with connective tissue cells, as well as immune cells. These immune cells include a number of different kinds of white blood cells located here to help protect the airways. However, in the case of asthma, this protective feature goes into overdrive, causing an inflammatory response that damages host tissue. The bronchioles are composed of a three-layer tube surrounded the lumen or air passageway. The innermost layer, closest to the lumen, is composed of ciliated columnar epithelial cells; the constant sweeping action of the cilia important to help clear the bronchial passageways of irritants, including infectious agents. This layer also contains mucus producing goblet cells; the mucus another important defense mechanism to trap irritants and microbes to prevent their passage into the alveoli. The middle layer, called the lamina propria, is embedded with connective tissue cells, as well as immune cells. These immune cells include a number of different kinds of WBCs, located here to help protect the airways. The outermost layer is composed of smooth muscle cells, responsible for the ability of the airways to constrict and dilate. alveolar hyperinflation with asthma, This image provides a visual of the some of the anatomical changes associated with chronic bronchitis. Note how the smooth muscle constriction, bronchial wall inflammation, and mucus plugs lead to another issue: alveolar hyperinflation. Because of the anatomical changes in the bronchioles associated with chronic irritation ventilation, especially exhalation, is compromised. Pressure differences during inhalation are high enough to force air into the alveoli. However, during exhalation the narrowing and collapse of the air passageways causes air to be trapped in the alveoli resulting in.  alveolar hyperinflation à expanded thorax  hypercapnia (CO2 retention) à respiratory acidosis polycythemia vera; Polycythemia vera (pol-e-sy-THEE-me-uh VEER-uh) is a slowgrowing blood cancer in which your bone marrow makes too many red blood cells. These excess cells thicken your blood, slowing its flow. They also cause complications, such as blood clots, which can lead to a heart attack or stroke The major characteristics shared by these disorders are (1) involvement of a multipotent hematopoietic progenitor cell, (2) overproduction of one or more of the formed elements of the blood in the absence of a defined stimulus, (3) dominance of a transformed progenitor cell over the nontransformed progenitor cells, (4) marrow hypercellularity or fibrosis, (5) cytogenetic abnormalities, (6) predisposition to thrombus formation and hemorrhage, and (7) spontaneous transformation to acute leukemia. mechanism of action of anticholinergic drugs to treat asthma Abstract. Acetylcholine binds to muscarinic receptors to play a key role in the pathophysiology of asthma, leading to bronchoconstriction, increased mucus secretion, inflammation and airway remodelling. Block acetocholine binding (primarily in the lung) bronchodilation through decrease Parasympathic response Cardiovascular: review concepts related to cardiac output, cardiac output, which is defined as the volume of blood ejected by each ventricle per minute. 5L/min cardiac contractility, Myocardial contractility represents the innate ability of the heart muscle to contract. The ability to produce changes in force during contraction result from incremental degrees of binding between different types of tissue, that is, between filaments of myosin and actin tissue. preload/ Preload is defined as the degree of myocardial fiber length stretch before contraction. The degree of stretch will be influenced by the end-diastolic ventricular volume (EDV), which, as defined earlier, is the amount of blood entering each ventricle during diastole (e.g. 120-130 mL). Preload is “loading” the heart with blood. Preload can be increased by CHF, hypervolemia (increased blood volume). A boater paddling in deeper water has the ability to take a bigger stroke, but also risk overstretching and taking more water than they can effectively displace. Preload can be decreased by cardiac tamponade (external pressure on the heart) or hypovolemia (e.g. hemorrhage, dehydration). A boater paddling in shallow water has less ability to take a big stroke and, as a result, not displace as much water as necessary. afterload, And finally, afterload, the amount of tension the ventricle must develop during systole to open the SL valves and eject blood into circulation. I like to refer to afterload as “unload”. So, in our canoe analogy, what type of force is the person working against to displace or “unload” the water they have loaded their oar with? Are they paddling upstream or downstream? Afterload is influenced by: ventricle wall thickness = muscle strength increased thickness (more muscle mass) = decreased tension/force required for ejection arterial pressure = resistance to ejection increased pressure (either in pulmonary or systemic vessels) = increased tension required for ejection ventricle chamber size = blood volume capacity increased chamber size = increased blood volume = increased tension required for ejection Afterload can be increased by systemic hypertension, valve disease, or COPD = pulmonary hypertension. Afterload can be decreased by hypotension or vasodilation, such as seen in shock. Systole the phase of the heartbeat when the heart muscle contracts and pumps blood from the chambers into the arteries. 1. /diastole, the phase of the heartbeat when the heart muscle relaxes and allows the chambers to fill with blood. heart valves (when they are open and closed; the production of S1 & S2), This prompts closure of the AV valves to prevent backflow of blood into the atria. The closure of the valves can be auscultated and corresponds to the first heart sound. As pressure builds in the ventricles from the blood volume, this pushes the semilunar valves open. Meanwhile, the muscle cells of the ventricles contract (ventricular systole) and 55-70% of the blood is “pumped” from the ventricles into pulmonary and systemic circulation. This volume of blood is referred to as the cardiac ejection fraction. As the ventricles empty, pressure drops in the ventricles, forcing closure of the semilunar valves to prevent backflow of blood into the ventricles. The closure of these valves can also be auscultated and corresponds to the second heart sound. The “ lub” is the first heart sound, commonly termed S1, and is caused by turbulence caused by the closure of mitral and tricuspid valves at the start of systole. The second sound,” dub” or S2, is caused by the closure of aortic and pulmonic valves, marking the end of systole. stenosis of the heart valves and effects; Aortic valve stenosis — or aortic stenosis — occurs when the heart's aortic valve narrows. This narrowing prevents the valve from opening fully, which reduces or blocks blood flow from your heart into the main artery to your body (aorta) and onward to the rest of your body. When the blood flow through the aortic valve is reduced or blocked, your heart needs to work harder to pump blood to your body. Eventually, this extra work limits the amount of blood it can pump, and this can cause symptoms as well as possibly weaken your heart muscle. Can lead to heart failure stroke volume, stroke volume, the volume of blood ejected by each ventricle/systole ↓ heart rate à longer fill time à ↑ stroke volume ↑ heart rate à shorter fill time à ↓ stroke volume Stroke volume itself can be determined by three factors: preload, contractility and afterload. Cor Pulmonale, Right Heart Failure (Cor Pulmonale) is defined as the inability of the RV to provide adequate blood flow into pulmonary circulation. Causes of RHF include: pulmonary disease, causing pulmonary hypertension (the most common cause); RV MI (weakening the muscle); RV hypertrophy (secondary to cardiac damage); pulmonary SLV or tricuspid valve damage (causing backflow of blood into RA or RV after ejection); secondary to left heart failure (from build-up of pressure in damaged LV) Since pulmonary hypertension is the most common cause of RHF, we will use it to outline the disease process. Keep in mind that regardless of the cause, the overall process outlined here will be the same. High pulmonary vascular pressure (↑ afterload) will necessitate ↑ RV contraction force– increased force to eject/unload the blood. Overtime, this will reduce the ejection fraction and the RV will be unable to eject the normal amount of blood. This will increase the amount of blood remaining in the RV and, as a result ↑ RV preload, so the RA will be unable to eject the normal amount of blood into the RV. This will increase the amount of blood remaining in the RA and ↑ RA preload. This causes back up of blood volume (and pressure) in the vena cava and systemic veins. Jugular vein distension is characteristic of RHF. Because of the large volume of blood flow through the liver and spleen, these areas become engorged, resulting in hepatosplenomegaly. Increased pressure will force fluid from the systemic capillaries into the peripheral tissues, essentially flooding those areas and resulting in peripheral edema. Unresolved RHF will increase pressure on the left side of the heart, contributing to L heart failure as well – a condition called “biventricular heart failure.”