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Medical report - Case Study Example

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Patient and Setting: RJ is a 56-year-old white male who presents to his primary care physician.  Chief Complaint: Shortness of breath occurring with minimal exertion  History of Present Illness: RJ complains of increasing shortness of breath with minimal exertion…
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Medical report
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?Patient and Setting: RJ is a 56-year-old white male who presents to his primary care physician.  Chief Complaint: Shortness of breath occurring withminimal exertion  History of Present Illness: RJ complains of increasing shortness of breath with minimal exertion. He reports symptoms of dispnea when walking up his driveway to the mailbox. By the time he returns to the house, he needs to rest for 10 minutes. These complaints are new within the past 4 months. He has used a Primatene Mist inhaler as self-medication but notices that it makes his heart race.  Medical History: Relatively unremarkable, except for benign prostatic hypertrophy and 2 episodes of acute bacterial prostatitis within the past 8 months. These resolved with courses of ciprofloxacin. Patient also reports chronic knee pain previously diagnosed as osteoarthritis. He uses acetaminophen for mild pain and ibuprofen with more significant pain and stiffness. He reports frequent symptoms of heartburn for which he uses Omeprazole intermittently. He has problems with insomnia since the death of this wife and uses Zolpidem occasionally (1-2 times per week).  Surgical History: Appendectomy at age 35  Family History: RJ is a widower who lives alone in a house that he owns. His wife died 3 years ago from lung cancer attributed to a 40 pack-year smoking history. One sister (age 63) is alive and has diabetes. Both parents are deceased. Father died in an automobile accident at age 68; mother died of breast cancer at age 54.  Social History: RJ has a 60 pack-year smoking history. He has smoked 1.5 to 2 packs per day for 35 years. He reports that he currently smokes 1 to 1.5 packs per day. Patient indicates that he has thought about stopping smoking but feels that there is too much stress right now for him to attempt it. He reports moderate alcohol use (glass of wine 3-4 times a week). He has one adult son (age 30) who is in good health and lives 2 hours away.  Medications: Tamsulosin 0.4 mg daily  Zolpidem 10 mg HS PRN  Acetaminophen 500 mg, 2 tablets every 4a€“6 hours if needed for pain  Ibuprofen 200 mg, 2-3 tablets every 6 hours if needed for pain  Epinephrine inhaler 220 I?g/puff, 2 inhalations every 6 hours  Omeprazole 20 mg daily (prn)  Aspirin 81 mg daily (for cardiac protection) Physical Examination:  GEN: Well-developed, well-nourished, obese white male who appears older than stated age; patient in mild respiratory distress  VS: BP 128/82, HR 88, RR 26, T 37.8A°C, Wt 102 kg, Ht 184 cm  HEENT: WNL, mucoid appearance to oropharynx  COR: RRR, no MRG  CHEST: No wheezing, distant crackles bilaterally in bases  ABD: Obese; BS present; no masses, guarding, or tenderness  GU: Prostate 1+ boggy, no nodules  RECT: WNL; stool guaiac 1+  EXT: No CCE  NEURO: A & O A— 3; DTRs intact and symmetrical  Results of Pertinent Laboratory Tests, Serum Drug Concentrations, and Diagnostic Tests:  Note lab numbers in parentheses are listed to highlight that a lab value may be represented in different units. Numbers in parentheses should correspond with the adjacent number for a lab value. For example, please note normal BUN is 10a€“20 milligrams per deciliter (mg/dL) or 3.6-7.1 millimoles per liter (mmol/L)  Na (sodium)135  K (potassium) 4  Cl (chloride)104  HCO3 23  Glucose 6.6 (119) BUN 4.6 (13)  Cr (Creatinine)123.8 (1.4) Hct (Hematocrit)0.42 (42) Hgb 136 (Hemoglobin)(13.6) Liver Function Panel:  AST 1.0 (60)  ALT 1.1 (64)  Alk Phos 2.5 (150)  GGT 70 (70)  LDH 3.2 (190)  T Bili 13.7 (0.8)  Spirometry: FEV1 2.5 L, Predicted 3.5 L  FVC 4 L, Predicted 4.2 L  Post Bronchodilator: FEV1 2.7 L  FVC 4.1 L  ABG: pH 7.36, pO2 8.6 (65), pCO2 6.0 (45), Bicarbonate 22, O2 sat 93%  Chest radiograph: consistent with COPD; mildly increased A/P diameter, flattening of diaphragms, diffuse scarring noted bilaterally; no evidence of acute infectious or malignant process  Drug/Non-Drug Plan for INSOMNIA related to depression: This patient has many other medical conditions that have much greater importance regarding his well being but nevertheless insomnia in COPD patients can lead to further worsening of the symptoms and general well being. Patients suffering from COPD are at increased risk of developing depression (Manen et al 2002). Also there are studies that show that depression is associated with increased incidence of insomnia but the opposite is also true because prolonged episodes of insomnia can lead to clinical manifestation of depression (Daniel 2008). This is important to be mentioned because insomnia is one of the common symptoms that are associated with COPD. Shortness of breath, nocturnal exacerbations of cough and oxygen desaturation, heart failure and other complications of COPD may cause difficulties in normal sleep patterns of the patients that eventually may lead to insomnia. However it is important to be mentioned that usage of benzodiazepines can compromise the respiratory function in these patients (Roth 2009). This is why we need a careful approach in treating symptoms of insomnia in these patients. Non-drug treatment of insomnia in COPD patients is found to be as effective as medication treatment, especially over a longer periods of time (6 months to 2 years) (Chesson et al. 1999). Some of the techniques of non-drug treatments are: - Stimulus control treatment – it is behavior treatment based on the assumption that insomnia is learned behavior that can be improved by avoidance of any activities in the bedroom that are not associated with sleeping (Morin et al. 1999). - Relaxation techniques – in order for the patient to relax before bed time. In this technique a biofeedback can be used in order to objectively asses the level of relaxation of the patient (Morin et al. 1999). - Paradoxical intention treatment – there are studies that show that fear of “not been able to sleep” is important factor for insomnia. Teaching the patient to learn to relax and stop “trying” to sleep is found to be beneficial in insomnia patients (Morin et al. 1999). - Sleep restriction treatment – this is another technique that tries to produce a mild sleep deprivation in the patient by limiting the amount of time he is sleeping that will eventually lead to faster sleeping onset (Morin et al. 1999). - Cognitive behavior psychotherapy – is multifactorial usage of the principles of the cognitive behavior psychotherapy to help the patients with insomnia (Morin et al. 1999). - Sleep hygiene is another method that tries to help the patient to prepare for bed-time, avoiding unnecessary excitation before sleeping, assuring comfort in the bed, pleasant room temperature and noise etc. (Edinger and Sampson 2003). Because of complexity of insomnia in COPD patients we must use drug and non-drug approach for optimal results. Non-benzodiazepine benzodiazepine receptor inhibitors (NBBRAs) are found to be effective in treatment of insomnia related to depression or COPD complications in COPD patients but in the same time by using NBBRAs we avoid the negative effect of benzodiazepine drugs on the respiratory function in COPD patients (Stege et al. 2008). - Zolpidem at 10mg before bedtime is found to have no negative effect on the levels of transcutaneus carbon dioxide or oxygen saturation during sleep in COPD patients (Christophe et al. 1996). - Nocturnal oxygen desaturation is another reason for impaired sleep and insomnia (Catterall et al. 1983). Usage of oxygen for reducing the nocturnal oxygen desaturation, or even usage of continuous positive airway pressure (CPAP) in patients with overlapping sleep apnea is found to have beneficial effect on the oxygen saturation during sleep and CPAP can help if the patient is diagnosed with sleep apnea (Catterall et al. 1983). This is of relevance to our patient because his BMI is 30.1 kg/m2 and there are studies that show that 60 to 90% of the patients with obstructive sleep apnea are obese (BMI above 29kg/m2) (Jonathan 2002). - Inhaled epinephrine that is frequently used by our patient can induce tremor, tenseness, nervousness, anxiety, restlessness and other symptoms that eventually can be the cause for insomnia (AHFS Drug Information 2010). Usage of selective beta2 agonists like Salbutamol is found that has no significant negative effects on the patterns of sleep in patients with COPD (Veale et al. 1994). Because of this stopping the usage of inhaled epinephrine and start of using inhaled beta 2 agonists may have beneficial effect on the insomnia of the patient. Plan to Monitor for INSOMNIA related to depression: As we discussed above insomnia in patients with COPD is caused by multiple factors. Depression is only one of the causative factors that may result in insomnia. Patient monitoring is important in order to develop effective and lasting solution for insomnia. There are studies that show that depression can be caused by insomnia, and because of this depression can be look as only a secondary complication from the insomnia in COPD patients. This is why we must monitor the general well being of the patient in order to effectively treat the symptoms of insomnia. - Patient should be under psychiatric monitor with regular examinations from psychiatrist in order to assess the psychological condition of the patient and assess the need for anti-depressive medication. - Patient should be monitored for his general symptoms regarding COPD – acute exacerbations, signs of sleep apnea and nocturnal oxygen desaturation, wheezing and other signs of worsening of its condition that will result in reduced night-coughs breathlessness, wheezing that can impair the sleep of the patient. - The therapy of the patient should be corrected and he should reduce the ussae of epinephrine inhaler that may result in sleeplessness and insomnia. Insomnia can result in significant reduction of the quality of life and sleep deprivation can be a cause of a number of psychiatric conditions, including depression (Ford 1989). In the case of our patient improving the general condition of the patient will result in improvement of his symptoms of insomnia and symptoms of depression he may have. What pharmacotherapy should be recommended for treatment of RJ’s main respiratory diagnosis? The patient in our case study has a number of medical conditions and he is taking drug therapy for these conditions. As we can see he is taking Tamsulosin a 0.4 mg propably for benign prostate hypertrophy symptom. He is also takin a number of pain medications: Ibuprofen, Paracetamol and additionally he is using Aspirin which is from the same NSAID group of drugs. These drugs caused heartburn and signs of gastritis and because of this the patient is taking proton pump inhibitor Omeprazole a 20 mg every day. However the main and most severe medical condition in this patient is COPD. He has a significant 60 pack-year smocking history which is a significant factor in developing COPD. The treatment for this condition must incorporate all aspects in order to be effective and have positive result: - Smoking cessation is first and maybe the most important factor in treating our patient. As we can see RJ has a 60 pack-years history of smocking and is still an active smoker. Patient must be put on a program for smoking cessation, taking a support groups, psychiatric counseling, usage of nicotine patches, usage of antidepressants and other available treatments that can be suggested by its physician or psychiatrist. - Inhaled beta 2 agonists must be introduced into the therapy of the patient. Selective beta 2 agonists like Salbutamol are administered in minute doses that have very small adverse effect in the organism but have many important positive effects in patients with COPD: they reduce the hyperinflation and predisposition to emphysema in COPD patients, they improve the FEV1 measurement and quality of life in COPD patients, they prevent nocturnal dispnea, improve the ventilation/perfusion ratio etc. (Belman et al. 1996) (Maclay et al. 2008). Short acting beta 2 agonists should be used for acute symptoms, and long acting beta 2 agonists should be prescribed for long term treatment. - Anticholinergic drugs are important in reducing the muscle tone in the bronchioles and by antagonizing the effect of acetylcholine on muscarinic receptors in the lungs. Usage of anticholinergic drugs in a number of studies has shown significant reduction in symptoms and severity of COPD in patients (Casaburi et al. 2002). RJ should be started on Ipratropium bromide 2-4 puffs 3 times a day. - Even though there are studies that show that inhaled corticosteroids are only modesly effective in patients with COPD compared with patients with ASTMA (Vestbo et al. 1999) there are studies that show that inhaled corticosteroids have synergistic effects with inhaled beta 2 agonists in patients with COPD (Calverley et al. 2007). This is why inhaled corticosteroid are routinely prescribed for the treatment of patients with COPD and our patient should be started on inhaled corticosteroid treatment. - Our patient is taking proton pump inhibitor (PPI) for his heart burn problems, but there are studies that show that PPI’s have beneficial effect on reducing the number and severity of COPD exacerbations (Sasaki et al. 2009). - Other treatments must also be taken into considerations in acute exacerbations of COPD, like antibiotic treatment, monolithic therapy, parenteral corticosteroids (Dexamethasone i.m.) etc. Are inhaled corticosteroids indicated for this patient? Why or why not?  As we mentioned above inhaled corticosteroids are not the mainstream treatment for COPD patients, however there are studies that show that inhaled corticosteroids improve the FEV1 measurement in patients with COPD but only slightly reduce the decline in FEV1 reduction in the same patients (Vestbo et al. 1999). However more importantly there are studies that have shown that combined therapy with inhaled corticosteroids and inhaled beta 2 agonits have synergistic effect and FEV1 improvement and broncho-dilatation is potentiated with combined use in patients with COPD (Calverley et al. 2007). This is why inhaled corticosteroid should be prescribed for the treatment of patients with COPD and our patient should be started on inhaled corticosteroid treatment. What is the potential influence of GERD on RJ’s main respiratory diagnosis?  As we mentioned above there are studies that show that PPI’s have beneficial effect on reducing the number and severity of COPD exacerbations (Sasaki et al. 2009). There are studies that there is increased incidence of GERD in patients with COPD which can cause aspiration of gastric fluid and onset of acute exacerbation of COPD (Casanova et al. 2004). This is why PPI should be recommended in patients and should not be discontinuated in our patient. Summarization of the therapeutic (drug and non-drug) modalities: Based on all of the discussions above we can conclude that treatment for this patient is complex and must include complex approach. We must consider the severity of his disease and use the appropriate treatment for the COPD. But also it is very important that we provide support and professional advice for this patient regarding several topics. Smoking cessation is one of the most important aspects of the treatment for this patient in order to stop the progression of the disease and reduce the exacerbations of COPD. Constant monitoring of the psychiatric condition of the patient may improve the quality of life for this patient and improve the compliance with the treatment and suggestions from the health professionals. However we must not forget that adequate drug therapy for this patient is crucial in order to improve the general well being and fitness of this patient. Further examination of the heart condition in order to exclude heart failure, atrial fibrillation or other heart condition that also contribute to exercional dispnea is recommended also. Using beta 2 agonists, anticholinergic drugs and inhaled corticosteroid is also recommended for better control of symptoms and improved lung function. References: J G van Manen, P J E Bindels, F W Dekker, C J IJzermans, J S van der Zee, E Schade (2002), Risk of depression in patients with chronic obstructive pulmonary disease and its determinants, Thorax - International journal of respiratory medicine, 2002;57:412-416 doi:10.1136/thorax.57.5.412 Daniel J. Tay (2008), Insomnia and Depression, Sleep, Associated Professional Sleep Societies, LLC. 2008 April 1; 31(4): 447–448, PMCID: PMC2279745 Roth T (2009), Hypnotic use for insomnia management in chronic obstructive pulmonary diseasе, Sleep Med. 2009 Jan;10(1):19-25. Epub 2008 Aug 9, PMID: 18693067 Stege G; Vos PJ; van den Elshout FJ; Richard Dekhuijzen PN; van de Ven MJ; Heijdra YF (2008), Sleep, hypnotics and chronic obstructive pulmonary disease, Department of Pulmonology, Rijnstate Hospital, PO Box 9555, 6800 TA, Arnhem, The Netherlands, Respir Med. 2008; 102(6):801-14 (ISSN: 0954-6111) Chesson AL Jr, Anderson WM, Littner M, et al. (1999), Practice parameters for the nonpharmacologic treatment of chronic insomnia. An American Academy of Sleep Medicine report. Standards of Practice Committee of the American Academy of Sleep Medicine. Sleep. 1999;22:1128-1133 Morin CM, Hauri PJ, Espie CA, Spielman AJ, Buysse DJ, Bootzin RR (1999), Nonpharmacologic treatment of chronic insomnia. An American Academy of Sleep Medicine review. Sleep. 1999;22:1134-1156 Edinger JD, Sampson WS (2003), A primary care "friendly" cognitive behavioral insomnia therapy. Sleep. 2003;26:177-182. Christophe Girault, MD; Jean-Frangois Muir, MD, FCCP;Florian Mihaltan, MD; Pascal Borderies, MD; Bertrand De La Giclais, MD; Annie Verdure, MD; and Dominique Samson-Dollfus, M (1996), Effects of Repeated Administration ofZolpidem on Sleep, Diurnal and Nocturnal Respiratory Function, Vigilance, and Physical Performance inPatients with COPD, Chest 1996;110; 1203-1211, DOI 10.1378/chest.110.5.1203 Catterall JR, Douglas NJ, Calverley PM, et al. (1983), Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome. Am Rev Respir Dis 1983;128:24-29 Jonathan L. Benumof, MD (2002), Obstructive sleep apnea in the adult obese patient: implications for airway management, UCSD Medical Center, Department of Anesthesiology, Anesthesiology Clin N Am20 (2002) 789– 81, 402 Dickinson Street (8812), San Diego, CA 92103-8812, USA AHFS Drug Information. (2010), Selected Revisions December 2008. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814, available online at: http://www.medscape.com/druginfo/monograph?cid=med&drugid=20017&drugname=EpiPen+IM&monotype=monograph&secid=4 Veale D, Cooper BG, Griffiths CJ, Corris PA, Gibson GJ. The effect of controlled-release salbutamol on sleep and nocturnal oxygenation in patients with asthma and chronic obstructive pulmonary disease. Respir Med. 1994;88:121-124 Ford DE, Kamerow DB (1989), Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA. 1989;262:1479-1484. Vestbo J, Sorensen T, Lange P, Brix A, Torre P, Viskum K (1999), Long-term effect of inhaled budesonide in mild and moderate chronic obstructive pulmonary disease: a randomised controlled trial, Lancet. 1999 May 29;353(9167):1819-23. Calverley PM, Anderson JA, Celli B, et al. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med. Feb 22 2007;356(8):775-89 Belman MJ, Botnick WC, Shin JW (1996), Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Mar 1996;153(3):967-75 Maclay JD, Rabinovich RA, MacNee W. Update in chronic obstructive pulmonary disease 2008. Am J Respir Crit Care Med. Apr 1 2009;179(7):533-4 Casaburi R, Mahler DA, Jones PW, et al. A long-term evaluation of once-daily inhaled tiotropium in chronic obstructive pulmonary disease. Eur Respir J. Feb 2002;19(2):217-24 Sasaki T, Nakayama K, Yasuda H, et al. A randomized, single-blind study of lansoprazole for the prevention of exacerbations of chronic obstructive pulmonary disease in older patients. J Am Geriatr Soc. Aug 2009;57(8):1453-7 C. Casanova, J.S. Baudet, M. del Valle Velasco, J.M. Martin, A. Aguirre-Jaime, J. Pablo de Torres and B.R. Celli et al. (2004), Increased gastro-oesophageal reflux disease in patients with severe COPD, European respiratory journall, doi: 10.1183/09031936.04.00107004, ERJ June 1, 2004 vol. 23 no. 6 841-845 Read More
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