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Cigarette smoke (CS) poses a significant risk factor for respiratory, vascular, and organ diseases owing to its high content of harmful chemicals and reactive oxygen species (ROS). These substances are known to induce oxidative stress, inflammation, apoptosis, and senescence due to their exposure to environmental pollutants and the presence of oxidative enzymes. The lung is particularly susceptible to oxidative stress (Cha et al., 2023). Smoking causes damage alveoli where the oxygen exchange occurs. In emphysema the alveoli coalesce to form a large cavity and the surface area available for gas exchange decreases. Chronic obstructive pulmonary disease (COPD) represents the fourth leading cause of morbidity and mortality in North America, in excess of 110,000 yearly deaths (Yoshida & Tuder, 2007).

           β-agonists up-regulate the transport of both sodium and chloride ions through the increase in intracellular cAMP caused by β-adrenoceptor stimulation (Bassford et al., 2012). β2-Agonists are effective bronchodilators due primarily to their ability to relax airway smooth muscle (ASM). They exert their effects via their binding to the active site of β2-adrenoceptors on ASM, which triggers a signaling cascade that results in a number of events, all of which contribute to relaxation of ASM (Rossi et al., 2008). Although β-agonists are bronchodilators some adverse events can occur such as increased heart rate and palpitations, because some of the β-ARs in the atria and ventricles are β2, and thus even selective β2-agonists can provoke direct simulation of the heart. Moreover, stimulation of β2-ARs can result in vasodilation and reflex tachycardia (Cazzola et al., 2013).

           Chronic obstructive pulmonary diseases (COPD), comprised of pulmonary emphysema, chronic bronchitis, and structural and inflammatory changes of small airways, is a leading cause of morbidity and mortality in the world. Smoking cigarettes induces cell death. Cigarette smoke has been associated with various molecular and cellular changes in the lung tissue, it has also been associated with lung and blader cancer as well as cardiac issues and complications. Smoke cessation is imperative to avoid any heart and long complications.

References

Cha, S.-R., Jang, J., Park, S.-M., Ryu, S. M., Cho, S.-J., & Yang, S.-R. (2023, June 3). Cigarette smoke-induced respiratory response: Insights into cellular processes and biomarkers. Antioxidants (Basel, Switzerland). https://pmc.ncbi.nlm.nih.gov/articles/PMC10295620/

Mannino, D. M. (2015, November). Smoking and emphysema – chest. Smoking and Emphysema. https://journal.chestnet.org/article/S0012-3692(15)50217-1/fulltext

Yoshida, T., & Tuder, R. M. (2007, July 1). Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease | physiological reviews. https://journals.physiology.org/doi/full/10.1152/physrev.00048.2006

Bassford, C. R., Thickett, D. R., & Perkins, G. D. (2012, March 20). The rise and fall of β-agonists in the treatment of ARDS – Critical Care. BioMed Central. https://ccforum.biomedcentral.com/articles/10.1186/cc11221#:~:text=%CE%B2-agonists%20up-regulate%20the%20transport%20of%20both%20sodium%20and,increase%20in%20intrac

Rossi, A. M., Khirani, S. M., & Cazzola, M. M. (2008, December 3). Long-acting beta2-agonists (LABA) in chronic obstructive pulmonary disease: Efficacy and safety. International journal of chronic obstructive pulmonary disease. https://pmc.ncbi.nlm.nih.gov/articles/PMC2650610/

Cazzola, M., Page, C. P., Rogliani, P., & Matera, M. G. (2013, January 10). Β 2 -agonist therapy in lung disease – ATS journals. β2-Agonist Therapy in Lung Disease. https://www.atsjournals.org/doi/full/10.1164/rccm.201209-1739PP

Emphysema, a hallmark of chronic obstructive pulmonary disease, is primarily caused by prolonged exposure to cigarette smoke, which leads to irreversible alveolar damage. Smoking initiates an inflammatory response characterized by increased neutrophils and macrophages, which release proteolytic enzymes such as elastase and matrix metalloproteinases (Barnes et al., 2020). These enzymes degrade elastin, an essential component of alveolar walls, resulting in the destruction of alveolar septa and the formation of enlarged air spaces. This structural damage reduces alveolar surface area, impairing gas exchange and leading to ventilation-perfusion mismatch. Additionally, smoking-induced oxidative stress further exacerbates lung injury by depleting protective antioxidants like glutathione, amplifying inflammation, and inducing apoptosis in epithelial and endothelial cells (Aghapour et al., 2021). Over time, emphysema results in progressive airflow limitation, hyperinflation, and reduced lung compliance, contributing to dyspnea and decreased exercise tolerance.

     β-Agonists are central to managing diseases with increased airway resistance, such as asthma and COPD. These drugs, primarily short-acting such as, albuterol and long-acting such as, salmeterol and formoterol, stimulate β2-adrenergic receptors on airway smooth muscle cells, leading to cyclic adenosine monophosphate activation and smooth muscle relaxation (Rabe & Celli, 2022). By reducing bronchoconstriction, β-agonists improve airflow and alleviate symptoms of wheezing and dyspnea. In addition to bronchodilation, these agents may modulate airway inflammation by inhibiting the release of pro-inflammatory mediators from mast cells and cytokines from immune cells. Their therapeutic role is particularly crucial in COPD, where chronic inflammation and mucus hypersecretion contribute to airway obstruction. Long-acting β-agonists, often combined with inhaled corticosteroids, enhance symptom control, reduce exacerbations, and improve quality of life for patients with obstructive lung diseases.

References

Aghapour, M., Raee, P., Moghaddam, S. J., Hiemstra, P. S., & Smit, J. J. (2021). Airway epithelial barrier dysfunction in chronic obstructive pulmonary disease: Role of cigarette smoke exposure. American Journal of Respiratory Cell and Molecular Biology, 64(2), 163-174. https://doi.org/10.1165/rcmb.2020-0244TR

Barnes, P. J., Baker, J., & Donnelly, L. E. (2020). Cellular senescence as a mechanism and target in chronic lung diseases. Nature Reviews Immunology, 20(12), 707-721. https://doi.org/10.1038/s41577-020-0370-1

Rabe, K. F., & Celli, B. R. (2022). Pharmacological treatment of chronic obstructive pulmonary disease: The ABCD revised. European Respiratory Journal, 59(2), 2100939. https://doi.org/10.1183/13993003.00939-2021

COVID-19 was a pandemic that took the entire world into its grip. Public education on the preventive measures, principally wearing a mask in public and enclosed spaces, was greatly emphasized before and after vaccination. How did consumer informatics play its role in having this message across the public? What role does social media play in sharing COVID-19 information with and among the public?  In which ways do Patient Portals play a role in creating healthcare awareness, increasing health literacy, and imparting health education? What challenges were encountered by public health professionals in employing these tools? Were the tools effective and efficient? Why? What could have been done to minimize the negative effects? 

Respond to a minimum two of your peers with a substantive comment assessing the proposed recommendations for the tools’ negative effects minimization. Follow APA formatting, referencing credible evidence. Only one outside source is allowed. Use the content of this class as the main source of evidence. 

Hypertension (HTN) is the leading cause of cardiovascular morbidity and mortality worldwide, and it raises the risk of stroke, heart disease, kidney failure, and other debilitating complications. The two major physiological factors that antihypertensive drugs target are cardiac output (CO) and peripheral resistance (PR) both play crucial roles in blood pressure control. By altering these determinants, these medications reduce the heart’s workload and prevent the long-term consequences of untreated HTN (Santisteban et al., 2023). Some antihypertensive medications result in reduced cardiac output, that is, the amount of blood expelled by the heart per unit of time. This is done with beta-blockers such as metoprolol or atenolol, which win and compete for beta-adrenergic receptors and thus reduce heart rate and myocardial contractility. It leads to a reduced stroke volume and, therefore, reduced cardiac output. Calcium channel blockers, such as diltiazem and verapamil (Hill et al., 2022), slow the heart rate and reduce contractility by blocking calcium influx into cardiac muscle cells, thus further decreasing cardiac output. Diuretics that have hydrochlorothiazide and furosemide reduce blood volume, resulting in the reduction of CO because they lower blood volume. They decrease preload and overall cardiac output by increasing the amount of sodium and water excreted by the kidneys, decreasing the fluid in the blood. Two additional classes of other antihypertensive drugs reduce peripheral resistance, or the force that opposes blood flow through the arterial system. Blocking the renin-angiotensin-aldosterone system (RAAS) is one of the predominant ways to achieve this (Budiarto et al., 2023). ACE inhibitors, lisinopril, enalapril, and angiotensin receptor blockers (ARBs), losartan, and valsartan prevent the action or formation of angiotensin II, a powerful vasoconstrictor. This causes the blood vessels to be relaxed, the vascular resistance to decrease, and the blood pressure to decrease. Moreover, calcium channel blockers like amlodipine and nifedipine cause direct vasodilation by inhibiting calcium entry into vascular smooth muscle, thereby inducing arterial relaxation and decreasing PR. Prazosin and doxazosin are alpha-blockers, and they work by blocking alpha-adrenergic receptors to stop them from vasoconstriction and maintain these dilated blood vessels. In more serious cases, direct vasodilators, either hydralazine or minoxidil can be given directly to vasodilate the vascular smooth muscle, rapidly decreasing the peripheral resistance and lowering blood pressure.

Untreated or undertreated hypertension can result in serious complications of multiple organ systems. In particular, the cardiovascular system is particularly vulnerable to these forces that continue for an extended period and take a strain on the heart, which then becomes hypertrophic, and this increases the risk of heart failure (Slone & Commodore-Mensah, 2024). Hypertension, therefore, predisposes to atherosclerosis and, subsequently, to myocardial infarction (heart attack), aortic aneurysm, and peripheral artery disease. With uncontrolled hypertension, there is an increased likelihood of ischemic and hemorrhagic strokes, where blood vessel damage to the brain is due to pressure ruptures or blocks. In addition, chronic hypertension is associated with vascular dementia and cognitive decline, as chronic hypertension induces cerebral perfusion (Yu et al., 2022). Another is the renal system. Suppose the glomeruli in the kidneys are damaged by high blood pressure in the long term. In that case, this may lead to chronic kidney disease (CKD) and, in the worst cases, to end-stage renal disease (ESRD), for which dialysis or transplantation is necessary. As well as the eyes, hypertension can cause hypertensive retinopathy (generated by hypertension that damages the retinal vessels, causing loss of vision or blindness). Furthermore, the peripheral vascular system is also in jeopardy because long-term hypertension can also lead to poor circulation, claudication (pain due to insufficient blood flow), and risk for limb ischemia. Because uncontrolled hypertension carries potentially life-threatening consequences, intervention, either pharmacologically, through meds, or in lifestyle, is essential early on. Prevention of complications and improvement of long-term health outcomes, therefore, requires regular blood pressure monitoring, adherence to antihypertensive medication, and lifestyle changes such as a healthy diet, routine exercise, smoking cessation, and stress reduction.

References

Budiarto, D., Wijianto, B., & Hariyanto, I. H. (2023). Study of anthocyanin molecule blocking as anti-hypertensive through the pathway of the renin-angiotensin-aldosterone system (RAAS). Indonesian Journal of Chemical Research, 11(1), 49-58. https://ojs3.unpatti.ac.id/index.php/ijcr/article/download/8131/5778

Hill, K., Sucha, E., Rhodes, E., Bota, S., Hundemer, G. L., Clark, E. G., … & Sood, M. M. (2022). Amiodarone, verapamil, or diltiazem use with direct oral anticoagulants and the risk of hemorrhage in older adults. CJC open, 4(3), 315-323. https://www.sciencedirect.com/science/article/pii/S2589790X21002997

Santisteban, M. M., Iadecola, C., & Carnevale, D. (2023). Hypertension, neurovascular dysfunction, and cognitive impairment. Hypertension, 80(1), 22-34. https://www.ahajournals.org/doi/abs/10.1161/HYPERTENSIONAHA.122.18085

Slone, S. E., & Commodore-Mensah, Y. (2024). Accurate Blood Pressure Measurement Is a Necessary but Insufficient Step to Diagnose and Control Hypertension. Circulation: Cardiovascular Quality and Outcomes, 17(2), e010738. https://www.ahajournals.org/doi/pdf/10.1161/CIRCOUTCOMES.123.010738

Yu, W., Li, Y., Hu, J., Wu, J., & Huang, Y. (2022). A study on the pathogenesis of vascular cognitive impairment and dementia: the chronic cerebral hypoperfusion hypothesis. Journal of Clinical Medicine, 11(16), 4742. https://www.mdpi.com/2077-0383/11/16/4742

In order to lower arterial blood pressure, antihypertensive drugs decrease cardiac output, total peripheral resistance or both. Diuretics, beta-blockers, and central adrenergic inhibitors decrease cardiac output. ACE inhibitors, angiotensin II antagonists, calcium antagonists, alpha-blockers, central adrenergic inhibitors, and after a delay also diuretics and beta-blockers decrease peripheral resistance (P; 2004). The cardiac stats of the hypertensive patient will affect which medication is given and how it will work for such patient. the indications for and criteria of treatment often must be adjusted according to the cardiac status of the patient. Thus, the presence of increased left ventricular (LV) wall thickness and mass in borderline hypertension may decide in favor of early treatment. The importance of systolic, as opposed to diastolic, blood pressure has been repeatedly stressed because of its closer relation to afterload and consequently of its more direct effects on cardiac performance (Adams et al., 2013). There are many cardiac factors that will affect the blood pressure, such as Reflex cardioadrenergic stimulation, which affect the increased output interfering with blood pressure control. Some side-effects that my apply are tachycardia, and coronary insufficiency, thus interfering with adequate therapy. Another sample is cardiac decompensation leading to further fluid retention and enhancing the increase in peripheral resistance. Reflex pressor effects coronary insufficiency leading to recurrent paroxysmal rises in blood pressure hypovolemia leading to orthostatic intolerance and vasovagal faints alterations in LV filling and relaxation, possibly leading to alterations in reflex blood pressure control (Adams et al., 2013).  Many patients can become resistant to such medicines and will ultimately need to be reevaluated for cardiac and hemodynamic status.

           Hypertension is termed when the blood pressure is above the normal range, that is 120/80mmHg. In older individuals, the blood pressure tends to be on the higher side usually due to the changes in blood vessel structure. In older individuals, of more than 60 years of age, a blood pressure of more than 140/90mmHg is considered hypertension (Adams et al., 2013). Many patients have hypertension and is goes unnoticed due to the fact they do not visit doctors or follow a poorly regimen with lack of exercise. Often stress can be another stressor to produce hypertension in adults. Renal failure also contributes to cardiac issues and hypertension as it is the second leading cause of renal failure with diabetes falling at number one in the world. Hypertension can damage the body for years producing damage and narrowing arteries, aneurysms. Coronary heart disease, enlarge disease, heart attack, etc. will damage the heart. TIA, and stroked will damage the brain. Kidneys and eyes as well as sexual conditions such as erectile dysfunction can occur due to untreated hypertension (Pruthi, 2023). High blood pressure usually is an ongoing condition that slowly causes damage over years if not treated, thus making yearly doctor visits and trying to live a healthy and less stressful life will always be beneficial to one’s health.

References

P; K. U. C. (2004, May 12). [pharmacological basis of antihypertensive drug therapy]. Praxis. https://pubmed.ncbi.nlm.nih.gov/15195836/

Adams, A. S., Uratsu, C., Dyer, W., Magid, D., O’Connor, P., Beck, A., Butler, M., Ho, P. M., & Schmittdiel, J. A. (2013, January 14). Health System factors and antihypertensive adherence in a racially and ethnically diverse cohort of new users. JAMA internal medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5105889/

Pruthi, S. (2023, November 28). How high blood pressure can affect the body. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/high-blood-pressure/art-20045868

Mary is a 70-year-old widow with a history of osteoarthritis. She has been self-medicating with over-the-counter acetaminophen, either extra strength (500 mg/tablet) or arthritis strength (650mg/tablet) for over a year now. In addition to osteoarthritis, she also has osteoporosis and gastroesophageal reflux. She presents with the complaint of backache and right knee pain, aggravated by climbing stairs. She describes her knee pain as 8 on a scale of 1 to 10: “I can stand the back pain, but the knee is awful.” She lives alone but has two supportive daughters nearby. They take her shopping and help with housework. On good days, she goes to the senior center for lunch and socialization. She was doing exercises at the Senior Center but stopped due to her knee pain. She does not smoke or drink alcohol, except at birthday parties and celebrations. She denies any medication, food, or environmental allergies. In addition to the acetaminophen, medications include calcium with vitamin D, Protonix (pantoprazole), and an annual intravenous infusion of Reclast (zoledronic acid). She also has been taking a dietary supplement of glucosamine/chondroitin for 3 months. She recently had a complete physical examination with electrocardiogram and laboratory tests and was told that everything was “normal.”

Susan is a 30-year-old registered nurse who works in transitional care. She presents to employee health stating, “My back is killing me. I was helping to transfer a patient and he moved. I thought he was going to fall, so I twisted around to grab onto him and wrenched my back. The pain is terrible, and I can barely walk.” Susan is a healthy young adult, married with a 5-year old. daughter. She has no significant family history. Susan has a past medical history of fractured coccyx as a teenager when she fell during cheerleading practice; no sequelae. She has smoked one-half pack of cigarettes a day since age 15 but is trying to quit. Current medicines include medroxyprogesterone acetate (Depo Provera) injection for birth control every 13 weeks. She is supposed to take calcium, but states that she “always forgets, and it constipates me anyway.” Susan denies any change in bowel/bladder habits.
 

EDUCATIONAL POWER POINT 

TOPIC IS HYPERTENSION 

• A description of the diagnosis and common symptoms using lay terms 
• A holistic treatment plan that includes: One medication and one evidenced-based non-pharmacologic treatment that is used for this diagnosis. Briefly explain how each will help the patient 
• As a provider briefly outline how you will assess SDOH in your plan of care (i.e. through motivational interviewing, engaging community health workers, etc.) LINK IS BELOW. Briefly explain how different SDOH can affect the patient’s health outcomes (housing, transportation, food security, healthcare access) 
• Appropriate resources for patients to get further information and/ or support 
• The last slide should include your references 

https://odphp.health.gov/healthypeople/priority-areas/social-determinants-health

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