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Immunology & Cancer: Exotoxins, Alloimmune Disorders, Hypersensitivity, & Cancer Risk, Exams of Nursing

An in-depth exploration of exotoxins and their impact on cell membranes and protein synthesis, as well as endotoxins and their role in the inflammatory response. It delves into alloimmune disorders, including transient neonatal disease and transplant rejection, and discusses the four types of hypersensitivity reactions. The document also covers live attenuated vaccines and their mechanism of action. Furthermore, it discusses various types of cancers, their risk factors, and associated complications, such as congestive heart failure and peripheral vascular diseases. Particularly useful for students studying immunology, microbiology, and cancer biology.

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2023/2024

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Download Immunology & Cancer: Exotoxins, Alloimmune Disorders, Hypersensitivity, & Cancer Risk and more Exams Nursing in PDF only on Docsity! NSG 530/NU 530 Quiz 2 Study Guide. NU 530 Quiz 2 Study Guide Chapter 8 Endotoxins are released when the bacteria die/ the are produced by gram-negative bacteria. Endotoxins released by blood-borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Bacteria injure cells by producing exotoxins or endotoxins. Exotoxins are enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis, and endotoxins activate the inflammatory response and produce fever. Gram-negative microbes produce an endotoxin (lipopolysaccharide [LPS]) that is a structural portion of the cell wall and is released during growth, lysis, or destruction of the bacteria or during treatment with antibiotics. Therefore, antibiotics cannot prevent the toxic effects of endotoxin. Bacteria that produce endotoxins are called pyrogenic bacteria because they activate the inflammatory process and produce fever. Septicemia is the proliferation of bacteria in the blood. Endotoxins released by blood- borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Leakage from vessels causes hypotension that can result in septic shock. Bacteremia occurs when bacteria are present in the blood. Gram-negative sepsis (sepsis or septicemia) occurs when bacteria are growing in the blood and release large amounts of endotoxin, when can cause endotoxic shock with up to 50% mortality. Released endotoxin, as well as other bacterial products, reacts with pattern recognition receptors (PRRs) and induces the overproduction of proinflammatory cytokines, particularly tumor necrosis factor- alpha (TNF-a), interleukin-1 (IL-1) and interleukin -6 (IL-6) which may secondarily be immunosuppressive. Endotoxin also is a potent activator of the complement and clotting system, leading to a degree of capillary permeability sufficient to permit escape of large volumes of plasma into surrounding tissue, contributing to hypotension and in severe cases, cardiovascular shock. Activation of the coagulation cascade leads to the syndrome of dissemination (or diffuse0 intravascular coagulation. Virulence: Capacity of a pathogen to cause severe disease (e.g., measles virus is a low virulence; rabies and Ebola viruses are highly virulent). https:// www.youtube.com/watch?v=9G1OELPrivU Attenuated vaccines: alive, but less infectious. Live attenuated vaccines are created by weakening infectious organisms that can still replicate and induce protective immune responses without causing disease in the host. Vaccination with the live but attenuated organism generates an immune response that protects the vaccinated person against severe disease or even infection. Available since the 1950s, live attenuated vaccines (LAV) Hypersensitivity is an immune response misdirected against the host’s own tissues (autoimmunity) or directed against beneficial foreign tissues, such as transfusions or transplants (alloimmunity); or it can be exaggerated responses against environmental antigens (allergy). NEED TO figure this out and break it down more Allergy means a hypersensitivity to environmental antigens. Immunity is the protective response to antigens. The four distinct types of hypersensitivity reactions: • Type 1 IgE allergic reactions o Type I (IgE-mediated) reactions occur after antigen reacts with IgE on mast cells, leading to mast cell degranulation and the release of histamine and other inflammatory substances. o Allergens are antigens that cause allergic responses, usually a type I hypersensitivity response. Some reactions are confined to the areas exposed to the antigen, such as the mucous membranes of the nose and eyes, causing symptoms of rhinorrhea, sneezing, and itchy, red, and watery eyes. Other reactions may involve all blood vessels and bronchiolar smooth muscle, causing widespread vasodi-lation, decreased cardiac output, and severe bronchoconstric-tion; this condition is known as anaphylaxis. • Type II tissue-specific reactions • Type III immune complex reactions Type III (immune complex–mediated) Immune complex disease can be a systemic reaction, such as serum sickness (e.g., Raynaud phenomenon), or localized, such as the Arthus reaction • TYPE I: RAPID HYPERSENSITIVITY REACTIONS Type I (rapid) hypersensitivity, sometimes called atopic allergy, is the most common type of hypersensitivity. This type results from increased production of the immunoglobulin E (IgE) antibody class. An acute inflammatory reaction occurs when IgE responds to an otherwise harmless antigen (e.g., pollen) and causes the release of histamine and other vasoactive amines from basophils, eosinophils and mast cells. ******Clinical examples of type I reactions include systemic anaphylaxis, allergic asthma, and atopic (genetic tendency) allergies such as hay fever, allergic rhinitis, and allergies to specific allergens such as latex, bee venom, TYPE II: CYTOTOXIC REACTIONS OVERVIEW In a type II (cytotoxic) reaction, the body makes special au-toantibodies directed against self-cells or tissues that have some form of foreign protein attached to them Clinical examples of type II reactions include Coombs'-positive hemolytic anemias, thrombocy-topenic purpura, hemolytic transfusion reactions (when an individual receives the wrong blood type during a transfu- sion), hemolytic disease of the newborn, Goodpasture's syndrome, and drug-induced hemolytic anemia There are many immune complex disorders (mostly connective tissue disorders) in which the type III reaction is the major mechanism of disease. For example, the clinical manifestations of rheumatoid arthritis are caused by immune complexes that lodge in joint spaces; this is followed by tissue destruction and, later, scarring and fibrous changes. • Type IV cell-mediated reactions Type IV (cell-mediated) reactions are caused by specifically sensitized T – lymphocytes cells, which either kill target cells directly or release lymphokines that activate other cells, such as macrophages. Anemia Lymphoede ma SLE Antigens Cell mediated Unlike with a type I hypersensitivity reaction, which occurs immediately, a type IV response typically occurs hours to days after exposure. Other clinical examples of type IV hypersensitivity reactions include contact dermatitis, poison ivy skin rashes, a local response to insect stings, allograft (tissue transplant) rejections, and granulomatous diseases in which the antigen is unknown (e.g., sarcoidosis). symptoms, such as destruction of red blood cells (anemia), lymphocytes (lymphopenia) and other cells, may be type II hypersensitivity reactions. Symptoms include: arthralgias or arthritis (90 %) , vasculitis and rash (70-80%) renal disease (40- 50%). Hematologic abnormalities (50%) – anemia most common complication and cardiovascular disease (30-50%). 11 Common Clinical Findings: Type II hypersensitivity in green 1. Facial rash confined to the cheeks (malar rash) 2. Discoid rash (raised patches, scaling) 3. Photosensitivity (Development of skin rash as a result of exospore to sunlight) 4. Oral or nasopharyngeal ulcers 5. Nonerosive arthritis of at least two peripheral joints 6. Serositis (inflammation of membranes of lungs [pleurisy] or heart [pericarditis]) 7. Renal disorders (persistent proteinuria of >0.5g/day or >3 on dipstick or cellular casts) 8. Neurologic disorders (seizures or psychosis in the absence of known causes) 9. Hematologic disorders, (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia) 10. Immunologic disorders (anti-double-stranded DNA ([sDNA] anti- Smith [Sm] antigen, false-positive serologic test for syphilis or antiphospholipid antibodies [Anticardiolipin antibody or lupus anticoagulant]) 11. Presence of antinuclear antibody (ANA) Laboratory diagnosis – positive ANA screening test: 98% of SLE test positive The presence of autoantibodies is a diagnostic criteria for SLE. Diagnostic criterion for SLE would include positive LE NO CURE HIV AIDS is an acquired dysfunction of the immune system caused by a retrovirus (HIV) that infects and destroys CD4+ lymphocytes (T-helper cells). Depletion of CD4+ cells – effect the immune system. HIV infection begins when a virion binds to CD4 Human immunodeficiency virus (HIV) infection and AIDS are associated with cardiac abnormalities, including myocarditis, endocarditis, pericarditis, and cardiomyopathy. Serologically negative (No detectable antibodies) Serologically positive (positive for antibody against HIV proteins) With a positive test – additional HIV protein testing (e.g. Western blot analysis) or HIV DNA (e.g. polymerase chain reaction) indicates infection by the virus. Stage 1: Acute HIV Infection Within 2 to 4 weeks after infection with HIV, about two-thirds of people will have a flu-like illness. This is the body’s natural response to HIV infection. Flu-like symptoms can include: • Fever • Chills • Rash • Night sweats • Muscle aches • Sore throat • Fatigue • Swollen lymph nodes • Mouth ulcers Stage 2: Clinical Latency • In this stage, the virus still multiplies, but at very low levels. People in this stage may not feel sick or have any symptoms. This stage is also called chronic HIV infection. • Without HIV treatment, people can stay in this stage for 10 or 15 years, but some move through this stage faster. Stage 3: AIDS If you have HIV and you are not on HIV treatment, eventually the virus will weaken your body’s immune system and you will progress to AIDS (acquired immunodeficiency syndrome). This is the late stage of HIV infection. The major immunologic finding in AIDS is the striking decrease in the number of CD4+T cells. Symptoms of AIDS can include: • Rapid weight loss = Cachexia includes anorexia, early satiety, weight loss, anemia, asthenia, taste alterations, and altered metabolism. • Recurring fever or profuse night sweats • Extreme and unexplained tiredness • Prolonged swelling of the lymph glands in the armpits, groin, or neck • Diarrhea that lasts for more than a week • Sores of the mouth, anus, or genitals • Pneumonia • Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids • Memory loss, depression, and other neurologic disorders mesenchymal tissue (including connective tissue, muscle, and bone). Chemical exposure. Being exposed to certain chemicals, such as herbicides, arsenic and dioxin, may increase the risk of soft tissue sarcomas. Radiation exposure. Leukemia is a cancer of blood- forming cells. Smoking, xrays, radiation, benzene, genetics Most common in Children Human papillomavirus (HPV) has been linked to cervical, anogenital, and penile cancers. Most common Sexually transmitted disease Direct skin contact Causes warts that may lead to cancer Cervical Cancer Human papillomavirus type 16 & 18 Know the different types of cervical cancer and how they are likely to be acquired -There are over 100 subtypes of HPV, and the virus is found in 99.7% of women with cervical cancer. HPV- 16 accounts for 50-60% of cervical cancer cases, followed by HPV-18 (10-12%) and HPV-31 and HPV-45 (4-5% each). HPV-16 is directly mutagenic by inducing the viral genes E6 and E7. Persistence of infection with high-risk HPV is a prerequisite for the development of cervical intraepithelial neoplasia. Hepatitis B and hepatitis C have been linked to the development of liver cancer, usually due to chronic inflammation. Epstein-Barr virus can lead to B-cell lymphomas in those patients who are immunosuppressed. Malignant tumors have no capsule, which allows them to spread readily. They have rapid growth rates and specific microscopic alterations. They are poorly differentiated and spread to distant tissues. Some tumors initially described as benign can progress to cancer and then are referred to as malignant tumors Malignant tumors have cells that vary in both size and shape, and they grow rapidly. Benign tumors are well encapsulated and well differentiated, but actually do retain some normal tissue. They do not spread to regional lymph nodes, nor are they generally resistant to treatment Point mutations are small changes in one or a few nucleotides. Tumor-suppressor genes encode proteins that in their normal state negatively regulate proliferation. Oncogenes are mutant genes that in their normal nonmutant state direct synthesis of protein that positively accelerates proliferation. Telomeres are protective ends, or caps, on each chromosome. Proto-oncogene is an oncogene in its nonmutant state. A cancerous tumor that is very poorly differentiated is referred to as being: Anaplastic (means the absence of differentiation) Excessive alcohol consumption is responsible for - Cancer of the oral cavity, larynx, pharynx, hypopharynx, esophagus, and liver. TNM staging – T = tumor N = nodes = M = metastases TNM numbers are grade or stage of cancer T Tumor T= primary tumor; the number equals size of tumor and its local extent Local tissue Breast T0 – Breast free of tumor T1-lesion <2cm in size T2-lesion 2-5cm T3- skin and/or chest wall involved by invasion N Nodes N = Lymph node involved, a higher number means more nodes are involved. N0 – No axillary nodes involved N1- Mobile nodes involved N2- Fixed nodes involved M Metastases M= extent of distant metastases M0- no metastases M1- demonstrable metastases M2- suspected metastases Metastasis is a complex process that requires cells to have many new abilities, including the ability to invade, survive, and proliferate in a new environment. Invasion consists of loss of cell-to-cell contact, degradation of the extracellular matrix (ECM), and migration of tumor cells to the vascular or lymphatic systems. Stromal cells, particularly tumor-associated macrophages (TAMs), are essential to this process. Hypertension is managed with both pharmacologic and nonpharmacologic methods that lower the blood volume and the total peripheral resistance. ACE – inhibitors, angiotensin receptor betablockers (ARBs). Diuretics (No other health issue) Which characteristics are associated with hypertension? (select all that apply) CORRECT • Family history positive for hypertension Hypertension is associated with positive family history, gender (men younger than 55 and women after menopause), black race, high dietary sodium, glucose intolerance, cigarette smoking, obesity, heavy alcohol consumption, and low dietary intake of minerals. Which complication occurs secondary to hypertension? • • Congestive heart failure Complications of hypertension include ventricular hypertrophy, angina pectoris, congestive heart failure, coronary artery disease, myocardial infarction, and sudden death PVD- presentation Peripheral vascular diseases include Buerger disease and Raynaud phenomenon, involving arterioles of the extremities Peripheral artery disease is the result of atherosclerotic plaque formation in the arteries that supply the extremities, and it causes pain and ischemic changes in the nerves, muscles, and skin of the affected limb. Common heart valve disorders and presenting symptoms- Mitral, aortic, rheumatic myocardial infarction- pathophysiology, causes, diagnostic workup Disorder Pathophysiology Causes Diagnostic workout Presenting symptoms Mitral valve Regurgitation causes left atrial and left ventricular dilation and hypertrophy Mitral regurgitation allows blood to flow from the left ventricle to the left atrium loud holosystolic murmur that radiates to the back and axilla Stenosis Left atrial hypertrophy and dilation Incomplete emptying of the left atrium Mitral stenosis would impair blood flow from the left atrium to the left ventricle Mitral stenosis has a rumbling-decrescendo murmur. Prolapse Most common cardiac valve disease in US Aortic valve Aortic Stenosis – Aortic stenosis has a Stenosis – causes left ventricular hypertrophy and dilation Aortic regurgitation Back flow into left ventricle Narrowing Pulse impairs blood flow from lef t ventricle to the aorta Aortic regurgitation allows blood to flow back into the left ventricle Widening pulse pressure & throbbing peripheral pulses crescendo- decrescendo murmur. Aortic regurgitation is associated with a water hammer pulse. Stenosis - Value opening constricted and narrowed Regurgitation – blood moves backwards into the chamber from where it came from. Disorder Pathophysiology Causes Diagnostic workout Presenting symptoms Rheumatic fever is an inflammatory disease that results from a delayed immune response to a streptococcal infection in genetically predisposed individuals. The disorder usually resolves without sequelae if treated early. The immune response cross-reacts with molecularly similar self-antigens in heart, muscle, joints, and the brain, causing an autoimmune response resulting in diffuse, proliferative, and exudative inflammatory lesions in these tissues. Valvular dysfunction is often related to rheumatic fever. Both stenosis and reger valve disorders A patient has rheumatic fever. Which valve is most commonly affected? Mitral The mitral valve is the most commonly affected in rheumatic heart disease. Severe or untreated cases of rheumatic fever may progress to rheumatic heart disease, a potentially disabling cardiovascular disorder. Acute rheumatic fever is characterized by carditis, acute migratory polyarthritis , chorea, and erythema marginatum, which occur 1 to 5 weeks after streptococcal infection of the pharynx Cardiac valve damage is caused by an abnormal immune response. Streptococci or other organisms cause the damage. Myocardial infarct: Sudden coronary Most common cause EKG – ST elevation Risk increases with low obstruction because of atherosclerosis of blood levels of HDL Myocardial ischemia may be asymptomatic, which is called silent ischemia, and is a risk factor for the development of the acute coronary syndromes. thrombus formation causes the acute coronary syndromes. These include unstable angina, non-ST elevation myocardial infarction (nonSTEMI), and ST elevation myocardial infarction (STEMI). coronary disease Clot formation at the site of rupture of an atherosclerotic plaque causes tissue ischemia which leads to an MI is blood flow is not restored. Myocardial infarction is caused by prolonged, unrelieved ischemia that interrupts blood supply to the myocardium. After about 20 minutes of myocardial ischemia, irreversible hypoxic injury causes cellular death and tissue necrosis. Cardiac troponins (Troponins I and T) are most specific elevations of the isoenzymes creatine kinasemyocardial bound (CK-MB), troponins, and lactate dehydrogenase 1 (LDH-1) and high levels of LDL A patient has a loud holosystolic murmur that radiates to the back and axilla. Which valvular abnormality is this describing? • Mitral regurgitation Which is the MOST common complication of an acute myocardial infarction (AMI)? • Arrhythmia All of these answer choices are true complications of AMI; however, the most common is arrhythmia. Ischemic heart disease is most commonly the result of coronary artery disease and the ensuing decrease in myocardial blood supply. Atherosclerotic plaque progression can be gradual and cause stable angina pectoris, which is predictable chest pain caused by myocardial ischemia in response to increased demand (e.g., exercise) without infarction. Which valvular disorder is characterized by impaired blood flow from the left atrium to the left ventricle? CORRECT • Mitral stenosis A patient experiences a rapidly progressive hypertension with a diastolic pressure of 146 mm Hg. Which is the correct term for this condition? 1. Hypertensive crisis (or malignant hypertension) is rapidly progressive hypertension in which diastolic pressure is usually greater than 140 mm Hg. It can occur in those with primary hypertension, but the reason why some people develop this complication and others do not is unknown. As hypertension becomes more severe and chronic, tissue damage can occur in the blood vessels and tissues leading to target organ damage in the heart, kidney, brain, and eyes. Which statement regarding cigarette smoke is correct? Cigarette smoking produces: CORRECT • an increased thrombotic state. There is an increase in the thrombotic state as well as in LDL level and inflammatory state but a decrease in HDL. Which statement regarding arteriosclerosis is TRUE? Arteriosclerosis is: CORRECT • thickening and hardening of the vessel wall. Arteriosclerosis is a chronic degeneration of blood vessel walls. Patho and presenting symptoms of genetic cardiac disorders including VSD, tetralogy of fallot, patent ductus arteriosus Genetic factors associated with congenital heart defects include, but are not limited to, Down syndrome, trisomy 13, trisomy 18, cri du chat syndrome, and Turner syndrome Congenital heart disease is the leading cause of death in the first year of life. There are 35 documented types of congenital heart disease. Thirty-five percent of deaths caused by congenital heart disease occur in the first year of life. The underlying cause is known in only 10% of cases. Disorder Patho Symptoms Ventricular septal defect (VSD) The most common type of congenital heart defect in infants. A hole in the septum between the two lower cardiac chambers (ventricles) A VSD has a harsh, loud, holosystolic murmur and systolic thrill. Tetralogy of fallot A heart shunt decreases flow through the pulmonary system, causing less than normal oxygen delivery to the tissues and resultant cyanosis. Infants with tetralogy of fallot experience cyanosis after crying or during feeding. Common is cyanosis and hypoxia A Tet spell is a hypoxic spell associated with the tetralogy of Fallot. Tetralogy of Fallot consists of four defects: a VSD that is high in the septum and usually large, the aorta is overriding and straddles the VSD, pulmonary stenosis, and right ventricular hypertrophy. Patent ductus arteriosus Coactation of aorta is narrowing of the aorta near the ductus arteriosus Weak or absent femoral pulses A patent opening between the aorta and pulmonary artery. Failure of the fetal ductus arteriosus to close, allowing blood to flow from the higher- pressure aorta to the lower-pressure pulmonary artery, causing a left-to-right shunt. The newborn will have weak or absent femoral pulses because blood flow is obstructed near the lower extremities. Most congenital heart defects begin to develop in the 8th week of gestation. The incidence of congenital heart disease (CHD) varies from 4 to 8 per 1000 live births and is the major cause of death in the first year of life other than prematurity. Several environmental and genetic risk factors are associated with the incidence of different types of CHD. Maternal conditions, such diabetes mellitus, increase the risk for CHD. Down syndrome has been associated with a relatively high incidence of heart defects. Congenital heart defects can be categorized according to (1) whether the defect causes cyanosis, (2) whether the defect causes increase or decrease blood flow into the pulmonary circulation, and (3) whether the defect causes obstruction of blood flow from the ventricles. An infant born with a congenital heart defect experiences sudden onset of dyspnea, cyanosis, and restlessness. Which condition will most likely be considered the cause of these symptoms? CORRECT “Tet” spell associated with tetralogy of Fallot A Tet spell is a hypoxic spell associated with the tetralogy of Fallot. Heart failure- pathophysiology, presenting symptoms, work up testing The most common causes of left ventricular failure are myocardial infarction and hypertension. The neuroendocrine mediators of heart failure include the sympathetic nervous system and the renin-angiotensin-aldosterone system; thus diuretics, beta-blockers, and angiotensinconverting enzyme (ACE) inhibitors are important components of the pharmacologic therapy. Diastolic dysfunction means that the left ventricular end-diastolic pressure is increased, even if volume and cardiac output are normal. Diastolic heart failure Right HF Ankle edema Jugular venous distention Hepatomegaly Potential cause – LHF Increases vascular resistance = Orthopnea Dyspnea Decreased urine output coughing pink frothy sputum Crackles on auscultation Myocardial dilatation Ventricular remodeling Left ventricular preload increases Pulmonary vascular congestion Left HF multiple trauma. acute, diffuse injury to the alveolocapillary membrane and decreased surfactant production, which increases membrane permeability and causes edema, atelectasis, and hypoxemia Hyperventilation/resp alkalosis Decreased tissue perfusion, metabolic acidosis, organ dysfunction Decreased tidal volume, hypoventilation Respiratory failure, < cardiac output, hypotension, death Restrictive Lung disease: Pulmonary edema is excess water in the lung caused by increased capillary hydrostatic pressure, decreased capillary oncotic pressure, or increased capillary permeability. Causes include left heart failure that increases capillary hydrostatic pressure in the pulmonary circulation, inflammation of alveoli, or lymphatic obstruction. Severe edema, pink frothy sputum is expectorated. Dullness to percussion over the lung bases, inspiratory crackles, and pink frothy sputum Dyspnea, hypoxemia Most common cause L sided heart failure Obstructive lung diseases: Asthma is an inflammatory disease of the airways resulting from a type I hypersensitivity immune response involving the activity of antigen, IgE, mast cells, eosinophils, and other inflammatory cells and mediators. Prolonged bronchospasm and server hypoxemia Inflammation, hypersecretion of mucus and bronchial smooth muscle constriction. Expiratory wheezes Reduced FEV1. Asthma episode that does not resolve with treatment – Status asthmaticus Long-term airway damage that is irreversible (Remodeling) Affects 10% of children birth – 17 years-old. Disease Presentation Workup PFT’s Extra Emphysema: destruction of the alveolar septa and loss Increased anterior- posterior chest diameter. (Barrel chest) FEVI (forced expiratory volume in 1 sec) goes down. Diagnosis is made by chest radiographs, thoracentesis, and sputum culture of passive elastic recoil And dyspnea lead to alveolar enlargement, airway collapse, obstruction of gas flow, and air trapping during expiration. Deep breath in and prolonged expiratory Use of accessory muscles to exhale Increased residual volume Thoarensintesis Sputum culture (Staphylococcus aureus) α¹ - Antitrypsin deficiency Chest xray – pus in pleural space Wheezing Clubbing of the fingers is a response to chronic hypoxemia. Pneumothorax- open and tension- presentation and labs Pneumothorax is air in the pleural space, can be spontaneous, iatrogenic or traumatic. 1. Spontaneous – rupture of an alveolus ▪ Most often in health adults 20 – 40 2. Iatrogenic – introduction of air into the pleural space ▪ ▪ Mechanical ventilation ▪ Thoracentesis ▪ Central line ▪ Lung biopsy 3. Traumatic – chest wound or rib fracture. Pneumothorax Presentation Labs Open A sucking sound would be heard without tracheal deviation Chest pain, dyspnea or asymptomatic (if small) Chest x-ray US CT Tension – air enters the pleural space but cannot exit ex. Penetrating chest wound Life threatening! Absent breath sounds, hypo tension, jugular venous distension Tracheal deviation Cystic fibrosis – lab results findings To help confirm diagnosis of cystic fibrosis – monitor Chloride in sweat (Sweat test) Pulmonary function test will decrease functional residual capacity. • Hypersecretion of mucus is a characteristic. There is hypersecretion of mucus. This mucus will hold on to bacteria. There is a chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years. It is increased in smokers. Which disorders can be the cause of pulmonary fibrosis? (select all that apply) • Acute respiratory distress syndrome (ARDS) • Tuberculosis • Inhalation of excessive amounts of coal dust • Rheumatoid arthritis Which factors will be influential in the development of aspiration pneumonia? (select all that apply) CORRECT • The amount of aspirate The amount, pH, size, and bacterial count all affect the outcome of aspiration pneumonia. Protein content has not been identified as a factor that increases risk. • pH of the material aspirated • Size of the particles aspirated • Bacterial content present in the aspirate • Which statement regarding bronchiolitis is TRUE? It is: • an inflammatory obstruction of small airways occurs. It is an inflammatory obstruction of small airways and bronchioles observed most commonly in children and is caused by a virus. It is seen in adults with chronic bronchitis. Which medical condition places a client at high risk for developing acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)? (select all that apply) CORRECT • Pneumonia Which medical condition places a client at high risk for developing acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)? (select all that apply) • Pneumonia • Burns • Sepsis Which information will the nurse include when educating a client regarding his or her diagnosis of empyema? (select all that apply) • It is the presence of pus in the pleural space. • A complication of respiratory infection often occurs. • Diagnosis is made by thoracentesis and sputum culture. Empyema is the presence of pus in the pleural space and is a complication of respiratory infection. Empyema occurs most commonly in older adults and children and usually develops as a complication of pneumonia. Breath sounds are decreased directly over the empyema. Diagnosis is made by chest radiographs, thoracentesis, and sputum culture. A patient is born with an α-antitrypsin deficiency. Which of the following conditions will most likely manifest? • Primary emphysema Primary emphysema is the only option that involves an α-antitrypsin deficiency. Which pathogen is consistently associated with nosocomial pneumonia? • . CORRECT • Pseudomonas aeruginosa All of the other choices are community acquired. Pseudomonas are commonly acquired in a hospital or nursing home. Which preventable medical condition is the leading cause of hospitalization among children? • Community-acquired bacterial pneumonia Community-acquired bacterial pneumonia is one of the leading causes of hospitalization and is prevented with polyvariant pneumococcal conjugate vaccine. Which symptoms would be characteristic of cystic fibrosis (CF)? (select all that apply) • Persistent cough • Pneumonia • Barrel chest • Wheezing Which are risk factors for the development of childhood asthma? (select all that apply) CORRECT • Black • Hispanics • Urban dwellers Asthma is the most prevalent chronic disease in childhood, affecting 10% of U.S. children between 5 and 17 years of age, with boys more often affected than girls. Populations most affected include black and Hispanic children, those living in an urban setting, ethnic minorities, and those of low socioeconomic status. Which statements should be included in information regarding the function of surfactant? Surfactant: (select all that apply) • is a lipid-protein mix produced by type II cells. • is found in the lining of the alveoli. • reduces alveolar surface tension. Surfactant is a lipid-protein mix produced by type II cells. It is critical for maintaining alveolar expansion and allows for normal gas exchange. It lines the alveoli and reduces surface tension, preventing alveolar collapse at the end of each exhalation. Which is TRUE regarding sudden infant death syndrome (SIDS)? • Young maternal age increases incidence. Infants of mothers younger than 20 years of age are more likely to die of SIDS. The peak age for SIDS is 3-4 months, and the incidence declines after that. There is a higher frequency in winter months. Less prenatal care and poverty are predictive factors.
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