Multidisciplinary team for COPD

 

—  Pulmonary rehabilitation

—  Medication Management

—  Dietary Management

—  Physiotherapy

—  Psychological Support

—  Social Support

—  Education and Self-Management

The multidisciplinary team approach was also applied to an elderly patient experiencing an exacerbation of COPD. Due to advanced age and frail health, managing COPD exacerbations becomes particularly challenging. The patient's respiratory function already compromised by COPD was further strained during the exacerbation, leading to severe dyspnea and increased vulnerability to infections.

 Multi-disciplinary Practitioners

—  Emergency Room (ER) Doctor

—  Pulmonologist

—  Respiratory Therapist

—  Primary Care Physician

—  Nurse

—  Pharmacist

—  Physical Therapist

—  Dietitian

—  Psychologist/Psychiatrist

—  Social Worker

—  Occupational Therapist

A multidisciplinary team (MTD) comprises a group of healthcare professionals proficient in diverse fields. They collaborate as a team to plan, propose, and execute management for complex medical conditions (Chew & Mahadeva, 2018). For this patient, the team members of MTD included the following members; 

First, an ER doctor attended the patient who provided him with initial and timely care for the patient's COPD exacerbation. Following this a pulmonologist was consulted who advised labs and made a proper diagnosis. He also directed the treatment plan. The team also included a respiratory therapist who provided crucial support with breathing exercises and oxygen therapy. 

Nurses administered the medications and monitored the health status of the patient closely, while pharmacists managed the medications required for symptom relief and management. The team also involved mental health professionals such as psychologists or psychiatrists who addressed any anxiety or depression associated with COPD. Similarly, a primary care physician was also consulted who ensured ongoing care and coordination. A dietitian provided a diet plan considering his age and nutritional requirements. 

Additionally, physical therapists were also made the part of multidisciplinary team so that they might provide a customized exercise programs to improve this patient's physical condition and mobility. Social workers were involved so that they might facilitate access to resources and community support in order to ensure a holistic care. This collaborative effort was mainly aimed to manage symptoms effectively, improve the patient's respiratory function, and enhance overall well-being.

Conclusion

—  A progressive lung condition requires a comprehensive and multidisciplinary approach

—  Severe exacerbation episodes specifies stage 4 disease

—  A collaborative effort involving healthcare professionals, patients, and caregivers, promoting lifestyle modifications and adherence to treatment plans is essential.

—  Educational initiatives and self-management must be focused.

—  Advances in treatment options and ongoing research offer hope for improved management and outcomes.

References

—  Abi Abdallah, G., Diop, S., Jamme, M., Legriel, S., & Ferré, A. (2024). Respiratory Infection Triggering Severe Acute Exacerbations of Chronic Obstructive Pulmonary Disease. International journal of chronic obstructive pulmonary disease, 19, 555–565. https://doi.org/10.2147/COPD.S447162

—  Bhatt, S. P., Balte, P. P., Schwartz, J. E., Cassano, P. A., Couper, D., Jacobs, D. R., Jr, Kalhan, R., O'Connor, G. T., Yende, S., Sanders, J. L., Umans, J. G., Dransfield, M. T., Chaves, P. H., White, W. B., & Oelsner, E. C. (2019). Discriminative Accuracy of FEV1:FVC Thresholds for COPD-Related Hospitalization and Mortality. JAMA, 321(24), 2438–2447. https://doi.org/10.1001/jama.2019.7233

—  Boesing, M., Ottensarendt, N., Lüthi-Corridori, G., & Leuppi, J. D. (2023). The Management of Acute Exacerbations in COPD: A Retrospective Observational Study and Clinical Audit. Journal of clinical medicine, 13(1), 19. https://doi.org/10.3390/jcm13010019

—  Chew, J., & Mahadeva, R. (2018). The role of a multidisciplinary severe chronic obstructive pulmonary disease hyperinflation service in patient selection for lung volume reduction. Journal of thoracic disease, 10(Suppl 27), S3335–S3343. https://doi.org/10.21037/jtd.2018.07.36

—  Craig, T. J., & Henao, M. P. (2018). Advances in managing COPD related to α₁ -antitrypsin deficiency: An under-recognized genetic disorder. Allergy, 73(11), 2110–2121. https://doi.org/10.1111/all.13558

—  Currie, G. P., & Douglas, J. G. (2006). Oxygen and inhalers. BMJ (Clinical research ed.), 333(7557), 34–36. https://doi.org/10.1136/bmj.333.7557.34

—  Elmenawi, K. A., Anil, V., Gosal, H., Kaur, H., Chakwop Ngassa, H., & Mohammed, L. (2021). The Importance of Measuring Troponin in Chronic Obstructive Pulmonary Disease Exacerbations: A Systematic Review. Cureus, 13(8), e17451. https://doi.org/10.7759/cureus.17451

—  Faner, R., Sobradillo, P., Noguera, A., Gomez, C., Cruz, T., López-Giraldo, A., Ballester, E., Soler, N., Arostegui, J. I., Pelegrín, P., Rodriguez-Roisin, R., Yagüe, J., Cosio, B. G., Juan, M., & Agustí, A. (2016). The inflammasome pathway in stable COPD and acute exacerbations. ERJ open research, 2(3), 00002-2016. https://doi.org/10.1183/23120541.00002-2016

—  Hikichi, M., Mizumura, K., Maruoka, S., & Gon, Y. (2019). Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke. Journal of thoracic disease, 11(Suppl 17), S2129–S2140. https://doi.org/10.21037/jtd.2019.10.43

—  Kotlyarov S. (2023). The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis. International journal of molecular sciences, 24(10), 8725. https://doi.org/10.3390/ijms24108725

—  Kukrety, S. P., Parekh, J. D., & Bailey, K. L. (2018). Chronic obstructive pulmonary disease and the hallmarks of aging. Lung India : official organ of Indian Chest Society, 35(4), 321–327. https://doi.org/10.4103/lungindia.lungindia_266_17

—  Labaki, W. W., Martinez, C. H., Martinez, F. J., Galbán, C. J., Ross, B. D., Washko, G. R., Barr, R. G., Regan, E. A., Coxson, H. O., Hoffman, E. A., Newell, J. D., Jr, Curran-Everett, D., Hogg, J. C., Crapo, J. D., Lynch, D. A., Kazerooni, E. A., & Han, M. K. (2017). The Role of Chest Computed Tomography in the Evaluation and Management of the Patient with Chronic Obstructive Pulmonary Disease. American journal of respiratory and critical care medicine, 196(11), 1372–1379. https://doi.org/10.1164/rccm.201703-0451PP

—  Leap, J., Arshad, O., Cheema, T., & Balaan, M. (2021). Pathophysiology of COPD. Critical care nursing quarterly, 44(1), 2–8. https://doi.org/10.1097/CNQ.0000000000000334

—  Love, M. E., & Proud, D. (2022). Respiratory Viral and Bacterial Exacerbations of COPD-The Role of the Airway Epithelium. Cells, 11(9), 1416. https://doi.org/10.3390/cells11091416

—  Mansoor, S., Obaida, Z., Ballowe, L., Campbell, A. R., Patrie, J. T., Byrum, T. D., & Shim, Y. M. (2020). Clinical Impact of Multidisciplinary Outpatient Care on Outcomes of Patients with COPD. International journal of chronic obstructive pulmonary disease, 15, 33–42. https://doi.org/10.2147/COPD.S225156

—  NICE (2019). Overview: Chronic obstructive pulmonary disease in over 16s: Diagnosis and management: Guidance. NICE. https://www.nice.org.uk/guidance/ng115

—  O'Reilly S. (2016). Chronic Obstructive Pulmonary Disease. American journal of lifestyle medicine, 11(4), 296–302. https://doi.org/10.1177/1559827616656593

—  Pilcher, J., & Beasley, R. (2015). Acute use of oxygen therapy. Australian prescriber, 38(3), 98–100. https://doi.org/10.18773/austprescr.2015.033

—  Rahi, M. S., Thilagar, B., Balaji, S., Prabhakaran, S. Y., Mudgal, M., Rajoo, S., Yella, P. R., Satija, P., Zagorulko, A., & Gunasekaran, K. (2023). The Impact of Anxiety and Depression in Chronic Obstructive Pulmonary Disease. Advances in respiratory medicine, 91(2), 123–134. https://doi.org/10.3390/arm91020011

—  Santos, N. C. D., Miravitlles, M., Camelier, A. A., Almeida, V. D. C., Maciel, R. R. B. T., & Camelier, F. W. R. (2022). Prevalence and Impact of Comorbidities in Individuals with Chronic Obstructive Pulmonary Disease: A Systematic Review. Tuberculosis and respiratory diseases, 85(3), 205–220. https://doi.org/10.4046/trd.2021.0179

—  Terzikhan, N., Verhamme, K. M., Hofman, A., Stricker, B. H., Brusselle, G. G., & Lahousse, L. (2016). Prevalence and incidence of COPD in smokers and non-smokers: the Rotterdam Study. European journal of epidemiology, 31(8), 785–792. https://doi.org/10.1007/s10654-016-0132-z

—  Thebault, J. L., Roche, N., Abdoul, H., Lorenzo, A., Similowski, T., & Ghasarossian, C. (2023). Efficacy and safety of oral corticosteroids to treat outpatients with acute exacerbations of COPD in primary care: a multicentre pragmatic randomised controlled study. ERJ open research, 9(5), 00057-2023. https://doi.org/10.1183/23120541.00057-2023

—  Wheaton, A. G., Liu, Y., Croft, J. B., VanFrank, B., Croxton, T. L., Punturieri, A., Postow, L., & Greenlund, K. J. (2019). Chronic Obstructive Pulmonary Disease and Smoking Status - United States, 2017. MMWR. Morbidity and mortality weekly report, 68(24), 533–538. https://doi.org/10.15585/mmwr.mm6824a1

Treatment COPD

 

—  Oxygen Inhalation

—  At 2L/min through a rate-limiting device

—  Bronchodilator

—  Salbutamol

—  Empirical Antibiotics

—  Injection ceftriaxone

—  Injection azithromycin

—  Steroid

—  Oral prednisone

Since patient had 87% oxygen saturation, so he needed supplemental oxygen (Pilcher, & Beasley, 2015). Oxygen was administered at a flow rate of 2 L/min through a Venturi mask. Patients with chronic diseases often become accustomed to using low levels of oxygen for their respiration. Therefore, high-flow oxygen is not advised, as it can greatly increase blood oxygen levels, which can lead to a loss of the drive to breathe and result in the development of hypercapnia (Currie & Douglas, 2006). For this reason Venturi mask was applied in order to limit the oxygen supply.

The use of high-dose bronchodilators is crucial for managing acute exacerbations. Salbutamol, a beta-2 adrenergic agonist, was administered to the patient via nebulization. Ipratropium can also be given, or both can be administered alternately. However, research has not yet proven their additive benefit (Boesing, Ottensarendt, Lüthi-Corridori, & Leuppi, 2023).

Evidence has found that oral steroid use is beneficial during an acute exacerbation, because it improves the function of lungs, diminishes hypoxemia, speeds up recovery, and decreases the relapse rate (Thebault et al., 2023).  According to NICE guidelines, oral steroids should be given for 7 to 14 days (NICE, 2019).

Diagnosis of COPD

 

—  CXR

—  Increased bronchovascular markings

—  Emphysematous lung

—  Complete Blood Count

—  White blood cell count of 15 400/μl

—  Haemoglobin of 10.0 g/dl

—  Platelet count 331×10³/μl

—  Neutrophils 1100 per mm³

—  Coagulation Profile

—  Prothrombin time (PT) : 11 seconds

—  Partial thromboplastin time (PTT): 0.9 seconds

In order to further diagnose the disease, chest x-ray was done which revealed increased bronchovascular markings and an emphysematous lung and these are the typical findings of a patient with advanced COPD. The patient's complete blood count revealed a white blood cell count of 15,400/μL, a hemoglobin level of 10.0 g/dL, neutrophils count of 1100mm⁻³and a platelet count of 331×10³/μL. These findings implied leukocytosis, which means patient was having an infection and anemia. The patient's coagulation profile was performed that showed a prothrombin time (PT) of 11 seconds and a partial thromboplastin time (PTT) of 0.9 seconds. These values were within normal limits, signifying that the patient's blood clotting function was normal. It means COPD had not yet caused coagulation abnormalities in this patient.  This is important for managing potential complications such as pulmonary embolism.

Symptoms of COPD

 

—  Symptoms

—  Worsening of dyspnoea

—  Cyanosis

—  Confusion

—  Examination

—  Auscultation of the chest:

—  Diminished breath sounds bilaterally

—  Mild expiratory wheezing

—  BP -140/90 mm

—  Pulse: 86/ minutes

—  RR: 25/minutes

—  Oxygen saturation 87%

—  PH: 7.43

—  Temperature 39 C

—  Pco2 – 43 mmHg

—  Po2 – 59 mmHg

—  HCO3 – 28.9 mmHg

This patient was suffering from worsening of dyspnea. COPD usually presents with difficulty in breathing along with feelings of chest tightness, cough, and increased sputum production. When exacerbation occurs, the symptom intensity increases. Furthermore, it can lead to confusion and exhaustion. More severe damage may lead to cor pulmonale (heart failure) and peripheral edema. Confusion, cyanosis and exhaustion are consequences of the reduced oxygen supply that occurs as the disease leads to decrease flow of air in the lungs. In the absence of sufficient oxygen, the body feels exhausted and tired. Additionally, when the chest of a COPD patient with advanced disease is auscultated, it typically reveals decreased breath sounds, increased percussion notes, and audible expiratory wheezes. Also, the chest becomes hyperinflated, and its expansion decreases. These findings were present in this patient.

Since oxygen saturation is < 94% on air, Arterial Blood Gas (ABG) analysis of the patient was done and it came out normal. Arterial blood gas (ABG) was done because it helps to measure the respiratory and metabolic status along with pH of the critically ill patients. However, patient’s temperature was high. Therefore, further evaluation was needed in the form of laboratory tests. The remainder of the physical examination was unremarkable.

Risk Factors for COPD

This patient was a retiree and had been struggling with his health for many years. He lived in a small town and had been a factory worker, constantly exposed to dust and chemical fumes. Additionally, he had been a heavy smoker for 30 years, a habit he picked up in his youth and found difficult to quit despite numerous attempts. He recently missed his dose of pneumococcal vaccines. This patient had several risk factors contributing to his COPD and its exacerbations.

—  Smoking

—  Primary risk factor

—  Old age

—  Increase age leads to decline in lung function

—  Occupational exposure

—  Dust, chemicals and fumes

—  Air population

—  Industrial pollutants

—  Vehicle emission

—  Biomass fuel

—  Infections

—  Bacterial and viral infections

—  Weather changes

—  Sudden change in humidity and temperature

—  Comorbidity

—  Cardiac diseases

—  Gastroesophageal reflex disease and

—  Diabetes

—  Emotional and stress factors

—  Anxiety and psychological stress

—  Genetic factors

—  alpha-1 antitrypsin deficiency

Smoking is the primary risk factor for COPD, significantly contributing to its development and progression (Wheaton et al., 2019). Cigarette smoke contains a large number of chemicals and oxidants. Smoking leads to the generation of reactive oxidant substances that produce inflammation in the airway and lungs (Kotlyarov, 2023). This inflammation persists even if a person has stopped smoking. Chronic inflammation results in structural remodeling due to a high number of inflammatory cells within the lungs and the subsequent injury and repair. Additionally, smoke chemicals weaken the immune system of the lungs, causing infection, inflammation, and narrowing and swelling of the air passages. This further destroys alveoli and air sacs (Kotlyarov, 2023).

Old age is another crucial factor because as the age increases, it leads to a natural decline in lung function. This particularly makes older adults like this patient more susceptible to COPD (Kukrety, Parekh, & Bailey, 2018). Similarly, occupational exposure like to dust, chemicals, and fumes also serve as a significant risk factor, chiefly for individuals who have worked in environments with poor air quality.

Air pollution, including industrial pollutants and vehicle emissions, further exacerbates the risk of developing COPD (O'Reilly, 2016). Additionally, exposure to biomass fuel, commonly used for cooking and heating in poorly ventilated areas, is a notable risk factor. Likewise, infections, both bacterial and viral, are common triggers for COPD exacerbations, leading to worsened symptoms and increased morbidity (Love, & Proud, 2022).

There are several other factors responsible for COPD exacerbation. For example, weather changes especially when weather suddenly changes in humidity and temperature, this can also precipitate COPD exacerbations. Comorbidities such as cardiac diseases, gastroesophageal reflux disease and diabetes can complicate COPD management and increase the frequency of exacerbations (Santos et al., 2022). The medical history of patient only included mild hypertension.

Emotional and stress factors including anxiety and psychological stress can negatively impact COPD symptoms and overall disease management (Rahi et al., 2023). This patient had been struggling with his health, which might cause him stress.

Besides, there is a genetic disposition too due to alpha-1 antitrypsin deficiency. It can cause onset of COPD even in people who never smoke or exposed to any pollution (Craig, & Henao, 2018). Genetic factor was not found in this case.

Understanding and managing these risk factors were crucial for improving his quality of life and preventing further health decline. 

Introduction COPD

 

Aim of Presentation

To critically evaluate the patient suffering from COPD in terms of its pathophysiology, etiologies, risk factors, diagnosis and complications.

To highlight the roles of various healthcare professionals, the importance of a multidisciplinary approach in improving patient outcomes and provide insights into the experiences of individuals affected by COPD.

To investigate the effectiveness of interventions provided by nurses in improving COPD patient’s and caregivers' understanding of the disease, enhancing self-management skills and ultimately improving quality of life outcomes.

Patient was having a debilitating lung condition that can cause significant morbidity and mortality.

A chronic patientà so there was a progressive airflow obstruction.

COPD is characterised by a reduced FEV₁/FVC ratio < 0.7.

It develops gradually over years and can become irreversible.

Patient was now showing acute exacerbation of COPD.

It has become third leading cause of death globally.

The patient is a known case of COPD, a chronic, debilitating lung condition and a major cause of morbidity and mortality worldwide. It is characterised by a decreased FEV₁/FVC ratio of less than 0.7 and is now believed to be the third leading cause of death globally (Bhatt et al., 2019).  As it develops gradually over several years, patients may progressively lose their lung function. This is evident in this patient, who now presented with acute exacerbation and severe respiratory distress.  Moreover, COPD is more common in men and smokers, and its incidence increases with age (Terzikhan et al., 2016).

Pathophysiology of COPD

Tissue destruction

Cellular senescence

Impairment of the defence mechanisms

Chronic inflammatory cells accumulation

Disturbance of the repair mechanisms

Genetic conditions

Exacerbation à increase in airway resistance, worsening of expiratory flow limitation (EFL) and prolonged lung emptying.

Mucosal oedema

Bronchospasm

Thickened sputum secretions

The molecular pathophysiology of COPD is associated with chronic inhalation of detrimental particles, like those present in cigarette smoking, cellular senescence and genetic conditions (Hikichi, Mizumura, Maruoka, & Gon, 2019). Cell signalling and antimicrobial activity are essential to maintain homeostasis. Nevertheless, when reactive oxygen species (ROS) get accumulated in an excessive amount, they destroy the DNA, proteins and lipids (Hikichi, Mizumura, Maruoka, & Gon, 2019). Research has revealed that certain cytokines also participate in the pathology of this disease. However, evidence that they are involved in the pathogenesis of COPD remains inconclusive (Faner et al., 2016). Additionally, In COPD, it has been seen that there is an inhibition of neutrophil apoptosis while there is a decrease in the phagocytic function of alveolar macrophages (Hikichi, Mizumura, Maruoka, & Gon, 2019). This brings about neutrophil-induced inflammation because of secondary necrosis. All of these factors lead to airway narrowing and loss of elastic recoil in the lungs, resulting in airflow restriction.

Exacerbation leads to greatly increase in airway resistance and worsening of expiratory flow limitation. This is mainly because of mucosal oedema, thickened sputum secretions and bronchospasm. Lung emptying becomes also affected i.e. it becomes prolonged (Leap, Arshad, Cheema, & Balaan, 2021). This explains the pathophysiology of COPD and its exacerbation in this patient.

Chronic Obstructive Pulmonary Disease (COPD) Coordinating Complex Care

 


A 71-year-old male with a history of severe COPD and long-term oxygen therapy presented to the emergency department with acute worsening of dyspnoea, cyanosis, and confusion, indicative of an exacerbation of COPD perhaps triggered by a respiratory infection.

Aim à to understand the coordinated complex care of patient suffering from Chronic Obstructive Pulmonary Disease (COPD).

What is COPD? Define it and explain the type, pathophysiology and progression of COPD in the patient.

Symptoms of COPD: the common symptoms and their impact on the quality of life of a patient.

Etiologies and Risk Factors: the primary causes of COPD, such as smoking, environmental factors and genetic predisposition. The risk factors that has increased the chance of developing COPD.

Complications associated with COPD such as acute exacerbation in this patient, in addition to other common complications like pulmonary hypertension, respiratory failure, Cor pulmonale, bacterial infections, side effects of medications used for its treatment, depression, anxiety, etc.

Elaborate the importance of a individual as well as collaborative approach in managing COPD, how MTD improves patient outcome, decision making and communication.

Patients and caregivers often have specific questions about COPD that nurses should be prepared to address. 

BIOCHEMISTRY TERM PAPER GUIDELINES

You will choose an enzyme that is not covered in our lecture material (stay away from any enzymes used in glycolysis, gluconeogenesis, TCA, ETC, and fermentation). You will want to find an enzyme that already has a published crystal structure available (there are, quite literally, thousands to choose from). Check due dates on the syllabus. First come, first serve, so let me know when you find one you want to study (via email)! You may need to use interlibrary loan to get certain articles, which take about 48-72 h to come through. If you need help with getting an interlibrary loan, let me know. • The paper will be 5-8 pages, 1.5 spaced, 1-inch margins, with 12-point font in either Calibri, Bodoni, Gaudy Old Style, or Times New Roman. Note: If you have 4.5 pages, that is not 5 pages. If you can’t get to 5 pages, you didn’t do enough research on your enzyme. You will be using at least 12 references. Use the following resources to find your references: 

§ NCBI and PDB websites 

§ SciFinder and Google Scholar 

§ Online journals (this is not considered an electronic resource) 

 § ExPASy/Uniprot website 

§ Books, hard copy journals, reviews, etc… from the library 

§ Other resources may be used if they come from a .edu or .gov website 

• You will have a separate references page that follows the ACS style guide (found in the library). This is not part of your page count. 

• Appendix A will include your primary protein sequence. This is not included in your page count and is located after your references page. 

• Appendix B will be the first page of each of your references. These are also not included in your page count. 

• All tables, graphs, and images should be included within the body of the text, should have captions, and should be appropriately sized. If you need help with the text wrapping feature in Word, please see me. If it is really oversized I will shrink it to an appropriate size and consider your page count from there. What’s “appropriate”? You’ll be looking at a lot of articles for this paper, and should be getting a feel for it by reading those, but you are welcome to come ask me if you need a second opinion. 

 • You should include as much of the below information as possible. If some information isn’t known, you need to address that in your paper. It’s possible some of the information will be available by only mixing and matching organisms. That’s fine, as long as you mention this in your paper. I highly recommend breaking your paper up into sections with the following subtitles: an introduction, purification information, structural information, enzymatic information, metabolic information, and a conclusion. If you want to include other information, you can add extra sections if necessary (or add to those below if appropriate). The sections should include: 

o Introduction: Why do we care about this enzyme? What’s the history of the enzyme? It is part of a bigger class of enzymes? This section should be a general introduction.

 o Purification information: What tissue/organism is commonly used to study and purify the enzyme? How is the enzyme purified? 

o Enzymatic information: How is enzyme activity measured? What are the Vmax and Km for the enzyme? Are there any inhibitors known? Is this enzyme a drug target? For what disease? What is the mechanism for the enzyme? 

o Structural information: What is the X-ray structure, the molecular mass, primary sequence, and active site structure? What is the quaternary structure? Where is it found? What is the primary sequence (attach in appendix A). 

 o Metabolic information: What is the big picture for this enzyme (is it part of a pathway)? Is the enzyme regulated? o Conclusion: Revisit your introduction here and summarize the paper. 

 • You will need to be analyzing the papers you read, not simply restating the data you find in them. You may find conflicting information for certain areas, so present those that are most recent and that have the best research to back them up

Side effects of cannabis

 

The use of cannabis has substantially reduced the use of conventional pain medications, chiefly opioids.

Cannabis may improve the efficacy of other pain medicines as well.

It prevents the cancer cells growth and enhances the action of chemotherapy

Studies have shown that cannabis can make the daily functioning and quality of life better, particularly for those with chronic pain. 

Medical cannabis is well tolerated and has few adverse effects.

Medical Cannabis and its Therapeutic Effects

 

ü  Cannabis is an effective intervention for chronic pain in adults. ü  Its active ingredients are ·         delta-9-tetrahydrocannabinol (THC) ·         cannabidiol (CBD)   ü  A huge number of evidence demonstrate the efficacy of cannabis’ use.   ü  Cannabis reliefs pain via its antihyperalgesic and antinociceptive effects.     ü  A growing body of clinical research have shown a clinically noteworthy lessening in pain with the use of cannabis.   ü  It has been useful in cancer-related pain, fibromyalgia, migraines, and other pain conditions. From 1975 to December 2023, there have been plenty of researches demonstrating that cannabis can help patients get relief from their pain.

Alleviation of chronic pain is by far the most prevalent reason provided by patients for using cannabis for medical purposes.