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NURS 5002 Case Study #4 Refer to Case Study Grading Guidelines and Grading Rubric for a complete description of requirements and grading criteria. To make the case study as real as possible, while you are working through the case study do not look ahead at the information provided. You are working in a Family Practice office and Cheryl, a 42 yo female with c/o wheezing and SOB is the next patient. Her chart reveals the following: PMH Acute bronchitis X2 UTIObesitySH?-1 ppd smokerSocial alcohol 2-3 cups coffee/day 2-3 diet soda/day Lives with boyfriend Works full-time FH Mother – HTN, GERD Father – HTN, asthma, DMMEDS Alesse PRN: AcetaminophenIbuprofen Famotidine NKDAAs you prepare for this visit what are your primary concerns? My initial concerns are her smoking status, obesity, and past history of bronchitis. FILLIN \* MERGEFORMAT Based on the medications listed, what are your concerns? She is currently on Famotidine which lets me know she suffers from GERD. My primary medication concern in with Alesse. Smoking and age are contraindications for oral contraceptives. This increases her risk for stroke, heart attack and emboli. Upon Assessment of the patient you find the following information: Cheryl is having trouble breathing with some wheezing since she has started walking this Spring to lose weight. She has been walking outside and started with about 10-15 minutes three times per week. When she started increasing her time walking she noticed it was getting harder to breathe and at times she would wheeze. She initially thought it was due to the warmer weather and her just being overweight. She has never really exercised and has a job that limits activity and is mostly at a desk. ROS - orthopnea, chest pain, dizziness, indigestion, diarrhea, N/V, recent weight change, HA, sore throat, + occasional cough more prominent while walking, productive at times with clear sputum, some ankle edema after walking, Physical Exam Patient is alert and oriented in NADEENT – PEERLA, posterior pharynx slightly red with postnasal discharge, nasal mucosa pink; no adenopathy appreciated; TMs without bulging or retractions bilaterallyHeart RRR without murmur, rubs or clicks; no carotid bruits auscultated; pedal pulses 1+, radial pulses 2+, ankles large with small amount of edema (non-pitting) Lungs sounds coarse but CTA bilat anterior and posterior Abdomen large, round, soft, non-tender; bowel sounds present x4 quads; no masses palpable; unable to palpate liver border; VSBP 132/84 P 86 RR 20 O2 Sat 98% Ht. 5’4” Wt. 195 lbs What other question(s) would you like to ask Cheryl to assist with your diagnosis? What other information would you like to have had? Questions that I would like to ask are; “How long have these symptoms been present?”, “When do you notice that your legs/feet are more swollen such as am or pm, how frequently?” “Do you experience any chest pain when exercising”?, “Do you have pain in your legs/feet”?, “Do you have excess mucus in the am?”, “Any other family history of respiratory or cardiac issues?”, “How many years have you been a smoker?”, “How long have you been on birth control”?, “Have you noticed redness or heat in your feet/legs”?, “How long do the episodes of wheezing and sob last”?DIFFERENTIATION OF DISEASE Add 4th potential disease based on symptoms. (may add other columns if needed) DISEASE #1 DISEASE #2DISEASE #3 Disease #4 CHF Asthma Bronchitis COPDPathophysiology “The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs. The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration.?This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients. The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy)”(Dumitru, 2017). “Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma. Airway inflammation in asthma may represent a loss of normal balance between two "opposing" populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-α, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation. A study by Gauvreau et al found that IL-13 has a role in allergen-induced airway responses” (Asthma, 2017).“During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis.A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase” (Fayaaz, 2017).“Chronic bronchitis can be categorized as simple chronic bronchitis, chronic mucopurulent bronchitis, or chronic bronchitis with obstruction. Mucoid sputum production characterizes simple chronic bronchitis. Persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as?bronchiectasis, characterizes chronic mucopurulent bronchitis” (Fayaaz, 2017).Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development. The pathogenic mechanisms are not clear but are most likely diverse. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells. Accelerated aging and autoimmune mechanisms have also been proposed as having roles in the pathogenesis of COPD.?[5,?6]Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this suggests, therefore, that neutrophils and macrophages are required for the development of emphysema.Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation. (Mosenifar, 2017)Signs/SymptomsShortness of breath (dyspnea) when you exert yourself or when you lie downFatigue and weaknessSwelling (edema) in your legs, ankles and feet.Rapid or irregular heartbeatReduced ability to exercisePersistent cough or wheezing with white or pink blood-tinged phlegmIncreased need to urinate at nightSwelling of your abdomen (ascites)Sudden weight gain from fluid retentionLack of appetite and nauseaDifficulty concentrating or decreased alertnessSudden,severe shortness of breath and coughing up pink, foamy mucusCoughing, especially at night or during exerciseDifficulty breathingChest tightnessShortness of breathWheezingCoughProduction of mucus which can be clear, white, yellowish-gray, green or rarely streaked with blood.FatigueSOBFever/ChillsShortness of breath especially during activitiesWheezingChest tightnessClearing of throatChronic cough that may produce mucusBluish lips or nail bedsLack of energyUnintended weight loss in later stagesSwelling in ankles and feetTreatments: Angiotensin-converting enzyme (ACE) inhibitors.?These drugs help people with systolic heart failure live longer and feel better. ACE inhibitors are a type of vasodilator, a drug that widens blood vessels to lower blood pressure, improve blood flow and decrease the workload on the heart. Examples include enalapril (Vasotec), lisinopril (Zestril) and captopril (Capoten). Angiotensin II receptor blockers.?These drugs, which include losartan (Cozaar) and valsartan (Diovan), have many of the same benefits as ACE inhibitors. They may be an alternative for people who can't tolerate ACE inhibitors.Beta blockers.?This class of drugs not only slows your heart rate and reduces blood pressure but also limits or reverses some of the damage to your heart if you have systolic heart failure. Examples include carvedilol (Coreg), metoprolol (Lopressor) and bisoprolol (Zebeta). Diuretics.?Often called water pills, diuretics make you urinate more frequently and keep fluid from collecting in your body. Diuretics, such as furosemide (Lasix), also decrease fluid in your lungs so you can breathe more easily. Aldosterone antagonists.?These drugs include spironolactone (Aldactone) and eplerenone (Inspra). These are potassium-sparing diuretics, which also have additional properties that may help people with severe systolic heart failure live longer. Inotropes.?These are intravenous medications used in people with severe heart failure in the hospital to improve heart pumping function and maintain blood pressure. Digoxin (Lanoxin).?This drug, also referred to as digitalis, increases the strength of your heart muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure symptoms in systolic heart failure. It may be more likely to be given to someone with a heart rhythm problem, such as atrial fibrillation. (Dumitri, 2017)Long-term asthma control medications,?generally taken daily, are the cornerstone of asthma treatment. These medications keep asthma under control on a day-to-day basis and make it less likely you'll have an asthma attack. Types of long-term control medications include:Inhaled corticosteroids.?These anti-inflammatory drugs include fluticasone (Flonase, Flovent HFA), budesonide (Pulmicort Flexhaler, Rhinocort), flunisolide (Aerospan HFA), ciclesonide (Alvesco, Omnaris, Zetonna), beclomethasone (Qnasl, Qvar), mometasone (Asmanex) and fluticasone furoate (Arnuity Ellipta).Leukotriene modifiers.?These oral medications — including montelukast (Singulair), zafirlukast (Accolate) and zileuton (Zyflo) — help relieve asthma symptoms for up to 24 hours.Long-acting beta agonists.?These inhaled medications, which include salmeterol (Serevent) and formoterol (Foradil, Perforomist), open the bination inhalers.?These medications — such as fluticasone-salmeterol (Advair Diskus), budesonide-formoterol (Symbicort) and formoterol-mometasone (Dulera) — contain a long-acting beta agonist along with a corticosteroid. Because these combination inhalers contain long-acting beta agonists, they may increase your risk of having a severe asthma attack.Theophylline.?Theophylline (Theo-24, Elixophyllin, others) is a daily pill that helps keep the airways open (bronchodilator) by relaxing the muscles around the airways. It's not used as often now as in past years.Short-acting beta agonists.?These inhaled, quick-relief bronchodilators act within minutes to rapidly ease symptoms during an asthma attack. They include albuterol (ProAir HFA, Ventolin HFA, others) and levalbuterol (Xopenex).Ipratropium (Atrovent).?Like other bronchodilators, ipratropium acts quickly to immediately relax your airways, making it easier to breathe. Ipratropium is mostly used for emphysema and chronic bronchitis, but it's sometimes used to treat asthma attacks.Oral and intravenous corticosteroids.?These medications — which include prednisone and methylprednisolone — relieve airway inflammation caused by severe asthma. They can cause serious side effects when used long term, so they're used only on a short-term basis to treat severe asthma symptoms. (Asthma, 2017)For patients with an acute exacerbation of chronic bronchitis, therapy with short-acting agonists or anticholinergic bronchodilators should be administered during the acute exacerbation. In addition, a short course of systemic corticosteroid therapy may be given and has been proven to be effective. In acute bronchitis, treatment with beta2-agonist bronchodilators may be useful in patients who have associated wheezing with cough and underlying lung disease. Little evidence indicates that the routine use of beta2-agonists is otherwise helpful in adults with acute cough.?Nonsteroidal anti-inflammatory drugs are helpful in treating constitutional symptoms of acute bronchitis, including mild-to-moderate pain. Albuterol and guaifenesin products treat cough, dyspnea, and wheezing.Among otherwise healthy individuals, antibiotics have not demonstrated any consistent benefit in the symptomatology or natural history of acute bronchitis.?Most reports have shown that 65-80% of patients with acute bronchitis receive an antibiotic despite evidence indicating that, with few exceptions, they are ineffective. An exception is with cases of acute bronchitis caused by suspected or confirmed pertussis infection. The most recent recommendations on whether to treat patients with acute bronchitis with antibiotics are from the National Institute for Health and Clinical Excellence in the United Kingdom. They recommend not treating acute bronchitis with antibiotics unless a risk of serious complications exists because of comorbid conditions. Antibiotics, however, are recommended in patients older than 65 years with acute cough if they have had a hospitalization in the past year, have diabetes mellitus or congestive heart failure, or are on steroids. (Fayaaz, 2017)The most essential step in any treatment plan for?COPD?is to stop all smoking. It's the only way to keep?COPD?from getting worse — which can eventually reduce your ability to breathe.Bronchodilators. These medications — which usually come in an inhaler — relax the muscles around your airways. This can help relieve coughing and shortness of breath and make breathing easier. Depending on the severity of your disease, you may need a short-acting bronchodilator before activities, a long-acting bronchodilator that you use every day or both.Inhaled steroids. Inhaled corticosteroid medications can reduce airway inflammation and help prevent exacerbations. Side effects may include bruising, oral infections and hoarseness. These medications are useful for people with frequent exacerbations of?COPD. Fluticasone (Flovent?HFA, Flonase, others) and budesonide (Pulmicort Flexhaler, Uceris, others) are examples of inhaled bination inhalers. Some medications combine bronchodilators and inhaled steroids. Salmeterol and fluticasone (Advair) and formoterol and budesonide (Symbicort) are examples of combination inhalers.Oral steroids. For people who have a moderate or severe acute exacerbation, short courses (for example, five days) of oral corticosteroids prevent further worsening of?COPD. However, long-term use of these medications can have serious side effects, such as weight gain, diabetes, osteoporosis, cataracts and an increased risk of infection. (Mayo, 2017)Complications: Heart failure can reduce the blood flow to your kidneys, which can eventually cause kidney failure if left untreated. Kidney damage from heart failure can require dialysis for treatment.The valves of your heart, which keep blood flowing in the proper direction through your heart, may not function properly if your heart is enlarged or if the pressure in your heart is very high due to heart failure.Heart rhythm problems (arrhythmias) can be a potential complication of heart failure.Heart failure can lead to a buildup of fluid that puts too much pressure on the liver. This fluid backup can lead to scarring, which makes it more difficult for your liver to function properly Signs and symptoms that interfere with sleep, work or recreational activitiesSick days from work or school during asthma flare-upsPermanent narrowing of the bronchial tubes (airway remodeling) that affects how well you can breatheEmergency room visits and hospitalizations for severe asthma attacksSingle episodes of bronchitis aren’t typically isn’t concerning. Bronchitis can lead to pneumonia and frequent occurences can indicate the development of COPD.Pneumonia occurs when bacteria or viruses enter the lungs, creating an infection. According to the?Centers for Disease Control and Prevention, bacterial pneumonia is the most common form of pneumonia in the United States. It’s ranked evenly with influenza as the eighth leading cause of death in the country. The illness is especially dangerous for those with a weakened pulmonary system, such as those who have COPD. For these people, pneumonia can further damage the lungs. This can lead to a chain reaction of illnesses that can weaken the lungs even further. This downward spiral can lead to a rapid deterioration of health in people with COPD.One of the most critical complications of COPD is heart failure. Because people with COPD have lower levels of oxygen in their bloodstream, their heart will often suffer. According to the?American Thoracic Society, this can result in severe pulmonary hypertension in a small percentage of patients (less than 10 percent). For many patients, treating COPD can help prevent the disease from progressing to the point where it causes heart failure. Unfortunately, because many of the symptoms of heart failure can be the same as those of COPD, it may be difficult for patients to recognize that they are having heart issues until it’s too late.Since COPD often can be attributed to smoking, it’s not surprising that people with COPD often develop lung cancer. However, researchers have actually pinpointed a connection between COPD and lung cancer that is separate from a person’s smoking history. This is most likely related to the chronic inflammation within the lung. Genetics may also play a role. Since lung cancer is often fatal, it’s important that people with COPD remove factors that further damage the lungs, especially smoking. (Faris, 2016)What is your choice of disease for the given scenario? (place X in the box)????What is the detailed rationale for the 4th potential disease that you chose? I chose COPD due to her smoking status and symptoms. Wheezing, shortness of breath with activity, edema, excessive cough and mucus production all leads to the diagnosis of COPD. Since COPD causes damage to the lung tissue, over time it becomes more difficult to exhale. Increased activity results in SOB and coughing since the airways have narrowed and the air becomes trapped. Why did you make your choice of disease/diagnosis? Give good rational for your decision. My reasoning for this decision is stated in the above question. COMPARISON OF MEDICATIONSAdd 3rd and 4th potential medications. (may add other columns if needed)MEDICATION #1 MEDICATION #2MEDICATION #3 MEDICATION #4Proventil HCAAerospan AugmentinSymbicortClass/Type of med BronchodilatorCorticosteroidAntibioticSteroid/BronchodilatorMechanism of Action Activation of beta2-adrenergic receptors on airway smooth muscle leads to the activation of adenylcyclase and to an increase in the intracellular concentration of cyclic-3',5'-adenosine monophosphate (cyclic AMP). This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. Albuterol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles. Albuterol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges. Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from mast cells in the airway. (Proventil, 2017)“Elicits potent glucocorticoid and weak mineralocorticoid effects; acts topically at site of deposition in the bronchial tree to inhibit inflammatory cells and release of inflammatory mediators” (Aerospan, 2017).“Clavunate potassium is an irreversible inhibitor of B-lactamases produced by both gram positive and negative bacteria. It prevents hydrolosis of amoxicillin resulting in extending the spectrum of amoxicillin to B-lactamase producing bacteria”(Amoxicillin, 2016).Budesonide: Anti-inflammatory corticosteroid; has potent glucocorticoid activity and weak mineralocorticoid activity. Formoterol: Long-acting selective beta2-adrenergic agonist with rapid onset of action; acts locally as bronchodilator; stimulates intracellular adenyl cyclase, which results in increased cyclic adenosine monophosphate levels, causing relaxation of bronchial smooth muscle and inhibition of release of mast cell mediators. (Symbicort, 2017)Indications Treating or preventing breathing problems in patients who have asthma or certain other airway diseases. It may be used to prevent breathing problems caused by exercise.“Aerospan Inhalation Aerosol is indicated for the maintenance treatment of asthma as prophylactic therapy in adult and pediatric patients 6 years of age and older. Aerospan Inhalation Aerosol is also indicated for asthma patients requiring oral corticosteroid therapy, where adding Aerospan Inhalation Aerosol may reduce or eliminate the need for oral corticosteroids” (Aerospan, 2017).To reduce the development of drugresistant bacteria and maintain the effectiveness of Augmentin (amoxicillin/clavulanate potassium) and other antibacterial drugs, Augmentin should be used only to treat infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. (Augmentin, 2017)“Symbicort 160/4.5 is indicated for the twice daily maintenance treatment of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD) including chronic bronchitis and emphysema. Symbicort 160/4.5 is the only strength indicated for the treatment of airflow obstruction in COPD” (Symbicort, 2017).Side Effects Shakiness in the legs, arms, hands, or feetTrembling or shaking of the hands or feetFast, irregular, pounding, or racing heartbeat or pulseDizzinessIrritabilityNauseaSleeplessnessTrouble holding urineDifficulty sleepingBody achesCongestionCoughDryness/sore throtFeverHeadacheHoarsenessPain/swelling around eyesSOBSneezingHives/WeltsItchingPainful intercourseRedness of skinRashThick, white vaginal dischargeBody achesChillsCough, fever, sore throatDifficulty breathingCongestion HeadacheLoss of voiceMuscle achesPain around eyesStuffy/runny noseTightness of chest/wheezingFatigueComplications The cardiovascular side effects have included palpitations, peripheral vasodilatation and reflex tachycardia with blood pressure increasing or decreasing. Albuterol in higher dosages has been reported to aggravate angina, myocardial ischemia, or cause atrial or ventricular arrhythmias. Musculoskeletal side effects have included tremors, particularly at higher dosages. Tolerance can develop to the tremorogenic effects. Severe muscle cramping may occur infrequently.Following doses of 15 mg albuterol (the active ingredient contained in Proventil HFA) via nebulizer, hyperkalemic patients on hemodialysis experienced a 0.9 mEq/L decrease in plasma potassium which was sustained for 6 hours. Albuterol may stimulate sodium-potassium ATPase, resulting in an intracellular shift of potassium.Psychiatric side effects have included psychoses presenting as auditory hallucinations and persecutory delusions. These effects are generally associated with higher dosages.Respiratory side effects have included paradoxical bronchospasm. (Proventil, 2017)The most commonly reported adverse reactions include pharyngitis, rhinitis, headache, sinusitis, and increased cough.[Ref]Very common (10% or more): Pharyngitis (up to 17.5%), rhinitis (up to 15.7%)Common (1% to 10%): Increased cough, sinusitis, epistaxis, bronchitis, laryngitis, voice alteration, cold symptoms, nasal congestion, sinus drainage, sinus infection, sneezing, sputum, wheezing, bronchospasm, dyspnea, head stuffiness, nasal irritation, sinus discomfort, sore throat, dry throatCommon (1% to 10%): Vomiting, dyspepsia, abdominal pain, diarrhea, gastroenteritis, nausea, oral moniliasis, upset stomach, heartburn, constipation, gas, abdominal fullness, glossitis, mouth irritation, phlegmVery common (10% or more): Headache (up to 13.8%)Common (1% to 10%): Migraine, taste perversion, weakness, numbness, hyperactivityCommon (1% to 10%): Neck pain, myalgia (Aerospan, 2017)In general, side effects have been classified as mild and transient. Less than 3% of patients in clinical trials discontinued treatment due to side effects. The most frequent adverse reactions associated with immediate-release formulations have included diarrhea/loose stools (9%), nausea (3%), skin rashes and urticaria (3%), vomiting (1%), and vaginitis (1%). Extended-release tablets have been most frequently associated with diarrhea (14.5%), vaginal mycosis (3.3%), nausea (2.1%), and loose stools (1.6%).Gastrointestinal side effects have included diarrhea, nausea, abdominal pain, vomiting, indigestion, gastritis, generalized abdominal cramps, stomatitis, glossitis, mucocutaneous candidiasis, enterocolitis, black "hairy" tongue, small intestinal motor disturbances, hemorrhagic colitis, and pseudomembranous colitis. Colitis and Clostridium difficile pseudomembranous colitis have been reported with amoxicillin.Hypersensitivity reactions have occurred in up to 10% of patients, and may present as a skin rash, urticaria, pruritus, angioedema, serum sickness-like reactions (urticaria or skin rash accompanied by arthritis, arthralgia, myalgia, and frequently fever), erythema multiforme, Stevens-Johnson syndrome (rarely), acute generalized exanthematous pustulosis, hypersensitivity vasculitis, exfoliative dermatitis, and toxic epidermal necrolysis. Anaphylaxis has been rarely reported (up to 0.2%). Hypersensitivity may play a role in some cases of amoxicillin-clavulanate-induced renal and hepatic toxicity. Urticarial rash, erythematous maculopapular rash, edema, hypotension, fever, eosinophilia, and dyspnea have been associated with hypersensitivity reactions to amoxicillin.Dermatologic side effects have included rash, fixed drug eruption, bullous pemphigoid, erythema multiforme, Stevens-Johnson syndrome, and exfoliative dermatitis. Amoxicillin rashes occur more frequently in patients with unrecognized infectious mononucleosis. This rash is not necessarily indicative of a lifelong amoxicillin hypersensitivity.Hepatic side effects have included moderate elevations in serum transaminases (ALT and/or AST). Hepatic dysfunction (including cholestatic jaundice and hepatitis, increases in ALT and/or AST, serum bilirubin, and/or alkaline phosphatase) has been reported infrequently. Rare cases of jaundice, ductopenia, cholestatic hepatitis, granulomatous hepatitis, hepatic necrosis, and hepatocellular damage have also been reported. Less than 1 death per approximately 4 million prescriptions has been reported worldwide. Hepatic cholestasis and acute cytolytic hepatitis have been reported with amoxicillin use.Hematologic side effects associated with penicillins have included thrombocytopenia, anemia, hemolytic anemia, thrombocytopenic purpura, eosinophilia, agranulocytosis, and leukopenia. These are believed to be due to hypersensitivity and are usually reversible when the drug is discontinued. Mild to moderate thrombocytosis has been reported in less than 1% of patients treated with amoxicillin-clavulanate and 3.6% of patients treated with the extended-release tablets. Purpura, pancytopenia, granulocytopenia, medullary aplasia, prolongation of prothrombin time, and transient neutropenia have also been reported. (Augmentin, 2017)As with other inhaled drugs containing beta2-adrenergic agents, Symbicort should not be used more often than recommended, at higher doses than recommended, or in conjunction with other medications containing LABA, as an overdose may result. Clinically significant cardiovascular effects and fatalities have been reported in association with excessive use of inhaled sympathomimetic drugs. Patients using Symbicort should not use an additional LABA (e.g., salmeterol, formoterol fumarate, arformoterol tartrate) for any reason, including prevention of exercise-induced bronchospasm (EIB) or the treatment of asthma or COPD. (Symbicort, 2017)What is your choice of trmt. for the given scenario? (place X in box)????Why did you make this choice for treatment? Give good rational for your decision My decision was mainly based on her smoking history. While her symptoms could fit for CHF as well, without proper cardiac history and testing, I could not definitively choose this diagnosis. Considering that her symptoms are exacerbated with activity, it leads me to COPD. This seems to be more of a chronic issue rather an acute which rules out bronchitis. She has a previous history of bronchitis which can lead to COPD. What are other potential choices you could make for treatment? In cases of COPD, treatment is mainly based on smoking cessation and self-care. I would recommend pulmonary rehab services and refer her to a pulmonologist for chronic care. Oxygen therapy would be offered as needed. What education will you provide your patient based on her treatment, diagnosis and disease prevention? Education is a critical part of the COPD diagnosis. First and foremost, smoking cessation is imperative. It is important to educate her that exacerbations will occur and proper management is needed. A moderate exercise regimen is helpful in improving respiratory status and decreasing heart disease. Weight loss is needed in order improve breathing and reduce cardiac problems. Proper hand washing techniques are important since a simple cold or respiratory infection can lead to exacerbations. Timely medical attention is needed in order to prevent illnesses from causing detrimental effects. COPD is not curable and is a progressive disease but with proper education and medications, it can be managed. REFERENCESAerospan HFA (flunisolide inhaled) dosing, indications, interactions, effects, and more. (2016, December 30). Retrieved March 24, 2017, from - FDA prescribing information, side effects and uses. (2017, March 2). Retrieved March 24, 2017, from - Clavunate Potassium. (2016). Retrieved March 24, 2017, from . (2017, March 22). Retrieved March 23, 2017, from - FDA prescribing information, side effects and uses. (2017, March 2). Retrieved March 24, 2017, from Side Effects in Detail. (2017, March 2). Retrieved March 24, 2017, from , L. (2017, January 06). Heart Failure. Retrieved March 21, 2017, from , S. (2016, September 29). Recognizing Serious COPD Complications. Retrieved March 23, 2017, from , J. (2017, February 09). Bronchitis. Retrieved March 23, 2017, from , J. (2017, February 09). Bronchitis Treatment & Management: Approach Considerations, Symptomatic Treatment, Antibiotic Therapy. Retrieved March 23, 2017, from failure Complications. (n.d.). Retrieved March 22, 2017, from Clinic Staff Print. (2016, July 12). Treatment. Retrieved March 23, 2017, from , Z. (2017, March 02). Chronic Obstructive Pulmonary Disease (COPD). Retrieved March 23, 2017, from HFA - FDA prescribing information, side effects and uses. (2017, March 2). Retrieved March 24, 2017, from HFA Side Effects in Detail. (2017, March 2). Retrieved March 24, 2017, from (budesonide/formoterol) dosing, indications, interactions, adverse effects, and more. (2017, March 23). Retrieved March 24, 2017, from - FDA prescribing information, side effects and uses. (2017, March 02). Retrieved March 24, 2017, from ................
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