NSG 5003 MIDTERM REVIEW

NSG 5003 Midterm Review Form of necrosis a/w TB? Caseous Most common cause of cellular injury? Hypoxia Acid- pH <7.35 Base- pH >7.45 Oxidative phosphorylation occurs in the mitochondria. Oxidative phosphorylation is the mechanism by which energy produced from carbs fats, and proteins is transferred to ATP. Hypotonic solution causes cellular swelling- D5W (dextrose in water), D5 1/2NS (5% dextrose and 0.45%NS), 1/2NS (0.45%NS), D5 1/4NS( 5% dextrose and 0.2%NS), 1/4NS (0.2%NS) Hypertonic solution causes cellular shrinkage- 3%NS “ocean water” Isotonic solution- LR, NS, D5NS Heat exhaustion- hemoconcentration from water and salt loss Water moves between the ICF and ECF compartments by osmosis. Water moves between the plasma and interstitial fluid by osmosis and hydrostatic pressure, which can occur across the capillary membrane. Hypokalemia- potassium <3.5 can be caused by reduced K+ intake, increased ICF to ECF K+ concentration, loss of K+, increased aldosterone secretion and increased renal secretion. S/S: decreased neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, cardiac dysrhythmias. Greatest carrier to push K+ back into the cell? Insulin Hypernatremia- Na+ > 147, can be caused by sodium gain or water loss. Movement of H20 from ICF to ECF. S/S: dehydration, convulsions, pulmonary edema, hypotension, tachycardia. TX: Isotonic salt-free fluids Hyponatremia- Na+ < 135, can be caused by Na+ deficits leading to plasma hypoosmolality and cellular swelling. S/S: lethargy, HA, confusion, apprehension, seizures, and coma. TX: fluid restriction, NaCl tablets Physical barriers? Skin, Ex: epithelial cells Mechanical barrier? Mucous membrane Biochemical barrier? Epithelial surfaces. Ex: mucus, sweat, saliva, tears, earwax Vascular injury is an acute inflammation that includes, vasodilation, increased capillary permeability, and WBC adherence to inner vessel walls and their migration through vessel walls. S/S/: redness, heat, swelling, and pain Neutrophils are the predominant phagocytes in the early inflammatory site, arriving within 6 to 12 hours after the initial injury, where they ingest (phagocytose) bacteria, dead cells, and cellular debris. Another population of granulocytes is the eosinophil. Eosinophils have two specific functions: (1) they serve as the body’s primary defense against parasites and (2) they help regulate vascular mediators released from mast cells. The second function, regulation of mast cell–derived inflammatory mediators, is a critical function of eosinophils. The basophil is the least prevalent granulocyte in the blood. It is very similar to mast cells in the content of its granules and, in addition, is an important source of the cytokine IL-4, which is a key regulator of the adaptive immune response. Although often associated with allergies and asthma, its primary role is yet unknown. The monocyte/macrophage is the predominant phagocyte in the late inflammatory response, is highly phagocytic, is responsive to cytokines, and promotes wound healing. Which statement is true regarding generation of clonal diversity? It occurs in primary lymphoid organs Active acquired immunity (active immunity) is produced by an individual either after natural exposure to an antigen or after immunization, whereas passive acquired immunity (passive immunity) does not involve the host’s immune response at all. Rather, passive immunity occurs when preformed antibodies or T lymphocytes are transferred from a donor to the recipient. This can occur naturally, as in the passage of maternal antibodies across the placenta to the fetus, or artificially, as in a clinic using immunotherapy for a specific disease. What is a foreign or non-self-substance? Antigen IgE? Primary cause of common allergies Examples of alloimmune diseases- Grave’s Disease, Myasthenia Gravis, Immune thrombocytopenia purpura, alloimmune neutropenia, and SLE. Hypersensitivity reactions require sensitization against a particular antigen that results in primary and secondary immune responses. An individual is sensitized when an adequate amount of antibodies or T cells is available to cause a noticeable reaction on re-exposure to the antigen. Immunogenicity: The ability of pathogens to induce an immune response Infectivity: The ability of the pathogen to invade and multiply in the host Pathogenicity: The ability of an agent to produce disease—success depends on communicability, infectivity, extent of tissue damage, and virulence Virulence: The capacity of a pathogen to cause severe disease—for example, measles virus is of low virulence; rabies virus is highly virulent Why antibiotic resistance occurs? Antibiotic resistance is usually a result of one of four general mechanisms resulting from genetic mutations that can be transmitted directly to neighboring microorganisms by plasmid exchange. • One mechanism microorganisms commonly develop is the capacity to inactivate antibiotics • Other forms of resistance result from modification of the target molecule • A third mechanism of resistance results from alteration of metabolic pathways that may be sensitive to antibiotics to alternative, more antibiotic-resistant pathways. • These transporters affect the rate of intracellular accumulation of the antimicrobial by preventing entrance or, more commonly, increasing active efflux of the antibiotic. Stress: General Adaptation System occurs in 3 stages: alarm stage, resistance or adaptation, and stage of exhaustion. The CNS, autonomic nervous system (ANS), endocrine system, and immune system are affected by stress. Endocrine system known as the hypothalamic-pituitary- adrenal system (HPA). In sequence, the hypothalamus secretes corticotropin-releasing hormone (CRH), which binds to specific receptors on pituitary cells that, in turn, produce adrenocorticotropic hormone (ACTH). ACTH is then transported through the blood to the adrenal glands located on the top of the kidneys. After binding to specific receptors on the adrenal glands, the glucocorticoid hormones (primarily cortisol; from the adrenal cortex) are released. Cortisol initiates a series of metabolic changes discussed in the section Glucocorticoids: Cortisol; however, overall, these hormones are thought to enhance immunity during acute stress and suppress immunity during chronic stress because of prolonged exposure and increased concentration.1 Parasympathetic Nervous system: The parasympathetic system balances the sympathetic nervous system and, thus, also influences adaptation or maladaptation to stressful events. The parasympathetic system also has anti-inflammatory effects. The parasympathetic system opposes the sympathetic (catecholamine) responses, for example, by slowing the heart rate. Sympathetic Nervous system: The sympathetic nervous system (SNS) is aroused during the stress response and causes the medulla of the adrenal gland to release catecholamines (80% epinephrine and 20% norepinephrine) into the bloodstream. Norepinephrine regulates blood pressure by constricting smooth muscle in all blood vessels. During stress, norepinephrine raises blood pressure by constricting peripheral vessels; it dilates the pupils of the eye, causes piloerection, and increases sweat gland action in the armpits and palms Epinephrine is rapidly transported to and acts on several organs, but it is metabolized quickly, making it short-acting. Metabolically, epinephrine causes transient hyperglycemia (high blood glucose level), decreases glucose uptake in the muscles and other organs, and decreases insulin release from the pancreas. Epinephrine has a greater influence on cardiac action and is the principal catecholamine involved in metabolic regulation. Epinephrine enhances myocardial contractility (inotropic effect), increases the heart rate (chronotropic effect), and increases venous return to the heart, all of which increase cardiac output and blood pressure. Epinephrine dilates blood vessels of skeletal muscle, allowing for greater oxygenation. Epinephrine in the liver and skeletal muscles is rapidly metabolized and dilates blood vessels supplying skeletal muscles, allowing for more oxygenation. Epinephrine also mobilizes free fatty acids and cholesterol by stimulating lipolysis, freeing triglycerides and fatty acids from fat stores, and by inhibiting the degradation of circulating cholesterol to bile acids. The metabolic actions of epinephrine aid the metabolic actions of cortisol, which are similar. Benign tumors, which are not referred to as cancers, are usually encapsulated and well differentiated. They retain some normal tissue structure and do not invade the capsules surrounding them or spread to regional lymph nodes or distant locations. Some tumors initially described as benign can progress to cancer and then are referred to as malignant tumors. These tumors are distinguished from benign tumors by their more rapid growth rates and specific microscopic alterations, including loss of differentiation and absence of normal tissue organization. One of the hallmarks of cancer cells, as seen under the microscope, is anaplasia, the loss of cellular differentiation, irregularities of the size and shape of the nucleus, and the loss of normal tissue structure. Cancers arising in epithelial tissue are called carcinomas, and if they arise from or form ductal or glandular structures are named adenocarcinomas. Cancers arising from connective tissue usually have the suffix sarcoma. Cancers of lymphatic tissue are called lymphomas, whereas cancers of blood-forming cells are called leukemias. Metastasis is the spread of cancer cells from the site of the original tumor to distant tissues and organs through the body. Metastasis is a defining characteristic of cancer, contributes significantly to the pain and suffering from cancer, and is the major cause of death from cancer. Cancers often spread first to regional lymph nodes through the lymphatics and then to distant organs through the bloodstream TUMOR MAJOR ANATOMIC PATHWAY COMMON SITE OF DISTANT METASTASIS Lung Pulmonary vein, left ventricle Multiple organs, including brain Colorectal Mesenteric lymphatics, portal venous system Liver Inferior vena cava, right ventricle, pulmonary artery Lungs Testicular Lymphatics to periaortic area to subclavian veins to right ventricle Lungs, liver, brain Prostate Regional lymphatics and veins, which drain to Batson plexus of presacral veins Bones (especially lumbar spine), liver Breast Axillary, transpectoral, and internal mammary lymphatics Bones, lung, brain, liver Head and neck Direct extension Lymphatics, liver, bones Ovarian Direct extension, peritoneal seeding, mesenteric veins Peritoneal surfaces, diaphragm, omentum, liver Sarcoma (extremity) Inferior vena cava, right ventricle, pulmonary artery Lungs Melanoma Regional lymphatics In transit lymphatics, lung, liver, brain, gastrointestinal tract If the diagnosis of cancer is established, it is critical to determine if the cancer has spread, known as the stage of the cancer. Staging initially involves determining the size of the tumor, the degree to which it has locally invaded, and the extent to which it has spread (metastasized). Cancer confined to the organ of origin is stage 1; cancer that is locally invasive is stage 2; cancer that has spread to regional structures, such as lymph nodes, is stage 3; and cancer that has spread to distant sites, such as a liver cancer spreading to the lung or a prostate cancer spreading to bone, is stage 4. One common scheme for standardizing staging is the World Health Organization’s TNM system: T indicates tumor spread, N indicates node involvement, and M indicates the presence of distant metastasis. Induction chemotherapy seeks to cause shrinkage or disappearance of tumors. Adjuvant chemotherapy is given after surgical excision of a cancer with the goal of eliminating micrometastases. Neoadjuvant chemotherapy is given before localized (surgical or radiation) treatment of a cancer. Radiation therapy is used to kill cancer cells while minimizing damage to normal structures. Ionizing radiation damages cells by imparting enough energy to cause molecular damage, especially to DNA. Radiation sources, such as small 125I-labeled capsules (also called seeds), can also be temporarily placed into body cavities, a delivery method termed brachytherapy. Brachytherapy is useful in the treatment of cervical, prostate, and head and neck cancers. Obesity and Cancer: Overall, the putative mechanisms whereby obesity drives the progression of cancer are not completely known and the process is complex. Earlier studies linked levels of circulating free hormones (e.g., estradiol) and hormonally driven cancers as an important mechanism. Consensus now exists that obesity is a risk factor for cancers of the endometrium, colorectum, kidney, esophagus, breast (postmenopausal), and pancreas. What we eat, how much we weigh, and how much we move influence our risks of developing cancer. Mounting evidence is clear—everyday choices impact our chances of getting or preventing cancer. Ongoing tedious and comprehensive investigative work is linking diet, body weight, and exercise to risk of specific cancers. Ultraviolet sunlight causes Basal cell carcinoma and Squamous cell carcinoma. Cardiac output is the volume of blood flowing through either the systemic or the pulmonary circuit and is expressed in liters per minute. Cardiac output is calculated by multiplying heart rate in beats per minute by stroke volume in liters per beat. Normal adult cardiac output at rest is about 5 L/min. The ventricles do not eject all of the blood they contain with each heartbeat and the amount ejected is called the ejection fraction. The ejection fraction is calculated by dividing the stroke volume by the end-diastolic volume. The end-diastolic volume (EDV) of the normal ventricle is about 70 to 80 ml/m2 and the normal ejection fraction of the resting heart is 55% or higher. Ejection fraction is a valuable clinical indicator of ventricular function. Four factors affect cardiac output directly: preload, afterload, myocardial contractility, and heart rate. Preload (pressure generated at the end of diastole) and afterload (resistance to ejection during systole) depend on the heart as well as the vascular system. Contractility and heart rate are characteristics of the cardiac tissue per se and are influenced by neural and humoral mechanisms Preload: Left ventricular preload is the pressure generated in the left ventricle at the end of diastole, or left ventricular end-diastolic pressure (LVEDP). It is determined by the left ventricular end-diastolic volume (LVEDV), which stretches the cardiac muscle fibers and in turn develops tension, or force, for contraction according to the Frank-Starling law. Preload is determined by two primary factors: (1) the amount of venous return to the ventricle, and (2) the blood left in the ventricle after systole or end-systolic volume. Afterload: Ventricular afterload is the resistance to ejection of blood from the ventricle. Aortic systolic pressure is a good index of afterload for the left ventricle. Low aortic pressures (decreased afterload) enable the heart to contract more rapidly, whereas high aortic pressures (increased afterload) slow contraction and cause higher workloads against which the heart must function to eject blood. Pressure in the ventricle must exceed aortic pressure before blood can be pumped out during systole. Increased aortic pressure is usually the result of increased peripheral vascular resistance (PVR), also called total peripheral resistance (TPR). Myocardial Contractility: Stroke volume, or the volume of blood ejected during systole, depends on the force of contraction, which is a function of myocardial contractility, the degree of myocardial fiber shortening. In healthy persons, three major factors determine the force of contraction: (1) changes in the stretching of the ventricular myocardium caused by variations in ventricular volume (preload), (2) alterations in nervous system input to the ventricles, and (3) adequacy of myocardial oxygen supply. A thrombus is a blood clot that remains attached to a vessel wall. A thrombus also has the potential of detaching from the vessel wall and circulating within the bloodstream (referred to as an embolus). Thrombophlebitis- inflammatory process that causes a blood clot to form and block one or more veins usually occurs in the leg. Patent ductus arteriosus: The patent ductus arteriosus (PDA) is a vessel located between the junction of the main and left pulmonary arteries and the lesser curvature of the descending aorta, usually just distal to the left subclavian artery. During fetal circulation the PDA allows blood to shunt from the PA to the aorta. At birth, once the placenta is removed and the lungs are expanded, the PDA will start to constrict within the first hours of life. Closure of the PDA in full-term infants is usually noted between 15 hours of life and 2 weeks of age. Failure of the PDA to close results in persistent patency of the ductus arteriosus. The hemodynamic effects of PDA depend on the size of the lumen and the resistance in the pulmonary and systemic circulations. At birth the pulmonary and systemic vascular resistances are almost equal and are reflected in the PA and aorta, respectively; therefore, shunting is minimal. However, as pulmonary vascular resistance falls, a reversal of fetal shunting occurs. Blood now begins to shunt left to right, from the aorta to the PA. The hemodynamic effect is increased pulmonary blood flow, resulting in increased pulmonary venous return to the LA and LV with increased workload on the left side of the heart. Patent Foramen Ovale allows right to left shunting. The foraman ovale is a hole in the walle between the left and right atria of every human fetus. The hole allows blood to bypass the fetal lungs, which cannot work until birth (exposed to air). When a newborn enters the world, and take their first birth, the foraman ovale close. Blood flow through the heart: The right and left sides of the heart are separated by portions of the heart wall called the interatrial septum and the interventricular septum. • Unoxygenated (venous) blood from the systemic circulation enters the right atrium through the superior and inferior venae cavae. From the right atrium the blood passes through the right AV (tricuspid) valve into the right ventricle. In the ventricle the blood flows from the inflow tract to the outflow tract and then through the pulmonic semilunar valve (pulmonary valve) into the pulmonary artery, which delivers it to the lungs for oxygenation. • Oxygenated blood from the lungs enters the left atrium through the four pulmonary veins (two from the left lung and two from the right lung). From the left atrium the blood passes through the left AV valve (mitral valve) into the left ventricle. In the ventricle the blood flows from the inflow tract to the outflow tract and then through the aortic semilunar valve (aortic valve) into the aorta, which delivers it to systemic arteries of the entire body. • The heart valves that ensure the one-way flow of blood from the atria to the ventricles are called the atrioventricular valves. The valves that ensure one-way flow from the ventricles to either the pulmonary artery or the aorta are called semilunar valves. • Oxygenated blood enters the coronary arteries through openings within the semilunar valves at the entrance to the aorta, and deoxygenated blood from the coronary veins enters the right atrium through the coronary sinus. • The pumping action of the heart consists of two phases: diastole, during which the myocardium relaxes and the chambers fill with blood; and systole, during which the myocardium contracts, forcing blood out of the ventricles. A cardiac cycle consists of one systolic contraction and the diastolic relaxation that follows it. Each cardiac cycle makes up one heartbeat. Tetralogy of Fallot (TOF) consists of four defects: a large VSD that is high in the septum, an overriding aorta that straddles the VSD, pulmonary stenosis (PS), and RV hypertrophy. • Pulmonary stenosis decreases blood flow to the lungs and, consequently, the amount of oxygenated blood that returns to the left heart. If blood also shunts from right to left through the VSD, deoxygenated blood mixes with the oxygenated blood returning from the lungs. The result is low oxygen saturation (hypoxemia) in the systemic circulation An atrial septal defect (ASD) is an abnormal communication between the atria. The three major types are: • an ostium primum defect, an opening found low in the septum that may be associated with AV valve abnormalities, especially mitral insufficiency; • an ostium secundum defect, an opening in the center of the septum (this is the most common type of atrial defect) • A sinus venosus defect, an opening that occurs high up in the atrial septum near the superior vena cava and RA junction. This defect is often associated with partial anomalous pulmonary venous connection. ASD: Although the pressure difference between the two atria is minimal, the ASD allows blood to be shunted from left to right because of the slightly higher pressure of the left atrial chamber and lower pulmonary vascular resistance as compared with systemic vascular resistance. Right atrial and ventricular enlargement develops as a result of left-to-right shunting. A ventricular septal defect (VSD) is an abnormal communication between the ventricles. The four types of VSDs are based on location in the septum. • The perimembranous type, which occurs in the outflow tract of the LV immediately below the aortic valve, is the most common type, accounting for up to 80% of all VSDs that require treatment. • Muscular VSDs, which occur low or anterior in the ventricular septum between the trabeculae are most likely to close spontaneously and are difficult to close surgically because of their location low in the ventricular apex. • Supracristal VSDs (also called outlet VSD) occur in the right ventricular outflow tract or infundibulum, below the pulmonary valve. • AV canal or inlet VSDs occur posterior and inferior to the membranous system, beneath the septal cusp of the tricuspid valve and inferior to the papillary muscles of the conus. VSD: The direction of shunting in a child with a VSD is from the high-pressure left side to the lower-pressure right side. After 1 to 2 weeks of life, when pulmonary vascular resistance has decreased, moderate-sized to large VSDs allow a large amount of shunting from left to right. The shunted blood flows directly out the RV outflow tract and into the PA rather than remain in the RV cavity. Therefore, the main PA, LA, and LV all enlarge. LV hypertrophy occurs to effectively pump the additional volume. Pulmonary overcirculation accounts for the symptoms associated with a large VSD in most cases. Pulmonary structure: The pulmonary system is made up of the upper airways, two lungs, the lower airways, and the blood vessels that serve them; the chest wall, or thoracic cage; and the diaphragm. The lungs are divided into lobes: three in the right lung (upper, middle, lower) and two in the left lung (upper, lower). Each lobe is further divided into segments and lobules. The space between the lungs, which contains the heart, great vessels, and esophagus, is called the mediastinum. A set of conducting airways, called bronchi, deliver air to each section of the lung. The lung tissue that surrounds the airways supports them, preventing their distortion or collapse as gas moves in and out during ventilation. The diaphragm is a dome-shaped muscle that separates the thoracic and abdominal cavities and is involved in ventilation. The nasopharynx, oropharynx, and related structures often are called the upper airway The larynx connects the upper and lower airways The trachea, which is supported by U-shaped cartilage, connects the larynx to the bronchi, the conducting airways of the lungs. The trachea divides into the two main airways, or bronchi, at the carina. The right and left main bronchi enter the lungs at the hila, or “roots” of the lungs, along with the pulmonary blood and lymphatic vessels. From the hila the main bronchi branch into lobar bronchi, then to segmental and subsegmental bronchi, and finally end at the sixteenth division in the smallest of the conducting airways, the terminal bronchioles. Gas exchange: The bronchioles terminate in gas-exchange airways, where oxygen (O2) enters the blood and carbon dioxide (CO2) is removed from it. The gas-exchange airways consist of respiratory bronchioles, alveolar ducts, and alveoli. These structures together are sometimes called the acinus, and all of them participate in gas exchange Respiration- the exchange of C02 for oxygen Ventilation is the mechanical movement of gas or air into and out of the lungs. Stridor- high-pitched sounds made during inspiration Wheeze- whistling sounds on expiration Rales- inspiratory crackles Kussmaul respirations are characterized by a slightly increased ventilatory rate, very large tidal volume, and no expiratory pause. Cheyne-Stokes respirations are characterized by alternating periods of deep and shallow breathing. Bronchiolitis is diffuse inflammation of the small airways or bronchioles. It is most common in children. S/S: a rapid ventilatory rate; marked use of accessory muscles; low-grade fever; dry, nonproductive cough; and hyperinflated chest. Chronic bronchitis is defined as hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year (usually the winter months) for at least 2 consecutive years. S/S: decreased exercise tolerance, wheezing, and shortness of breath. Individuals usually have a productive cough (“smoker’s cough”), and evidence of airway obstruction (decreased FEV1) is shown by spirometry. Hypoxemia may occur with exercise. As the disease progresses, copious amounts of sputum are produced, accompanied by frequent pulmonary infections. Asthma is a chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constriction of the airways, and variable airflow obstruction that is reversible. S/S: At the beginning of an attack, the individual experiences chest constriction, expiratory wheeze, nonproductive cough, dyspnea, prolonged expiration, tachycardia, and tachypnea. Severe attacks involve the use of accessory muscles of respiration, and wheezing is heard during both inspiration and expiration, and a pulsus paradoxus may be noted. Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) represents a spectrum of acute lung inflammation and diffuse alveolocapillary injury. All disorders that result in ARDS cause acute injury to the alveolocapillary membrane producing massive pulmonary inflammation, increased capillary permeability, severe pulmonary edema, shunting, mismatch, and hypoxemia. ARDS is often referred to as noncardiogenic pulmonary edema. ARDS progresses through three overlapping phases characterized by histologic changes in the lung: exudative (inflammatory), proliferative, and fibrotic. • Exudative (Inflammatory) stage- within 72 hours • Proliferative phase- 4-21 days • Fibrotic phase- 14-21 days • The clinical manifestations of ARDS are progressive as follows: • Dyspnea and hypoxemia with poor response to oxygen supplementation • ↓ • Hyperventilation and respiratory alkalosis • ↓ • Decreased tissue perfusion, metabolic acidosis, and organ dysfunction • ↓ • Increased work of breathing, decreased tidal volume, and hypoventilation • ↓ • Hypercapnia, respiratory acidosis, and worsening hypoxemia • ↓ • Decreased cardiac output, hypotension, and death Main bacteria in hospital acquired pneumonia? Pseudomonas aeruginosa Main bacteria in community acquired pneumonia? Streptococcus pneumoniae Cystic Fibrosis: is an autosomal recessive inherited disorder that is associated with defective epithelial chloride ion transport. The CF gene is located on chromosome 7. CF is characterized by abnormal secretions that cause obstructive problems within the respiratory, digestive, and reproductive tracts. However, research suggests that there may be additional CF-associated primary defects, such as an intrinsic proinflammatory state and abnormal local immune defenses in the lungs. The disease process causes progressive bronchiectasis. S/S: Respiratory symptoms include persistent cough or wheeze, sputum production, and recurrent or severe pneumonia. More subtle respiratory tract presentations of CF include chronic sinusitis and nasal polyps. Digital clubbing may appear quite early even in the absence of significant pulmonary impairment. Development of barrel chest or persistent crackles occurs much later during the disease. Otitis media is an infection of the middle ear and is the most common infection of infants and children. Most children have one episode by 3 years of age. The most common pathogens are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis Acute Otitis Media- s associated with ear pain, fever, irritability, inflamed tympanic membrane, and fluid in the middle ear. The tympanic membrane progresses from erythema to opaqueness with bulging as fluid accumulates. Chronic Otitis Media- persistent or recurring infection of the middle ear. Placement of tympanostomy tubes is considered when bilateral effusion persists for 3 months and for significant hearing loss.