Reply to Classmate COPD and pulmonary embolism

The revision that you did on my previous paper was great those are the types of papers I am looking for because this is a maters class. Below I have pasted 2 separate discussions that classmates posted. I have to reply to both. The first one is about pulmonary embolism and the second one is about COPD. I need 2 references in APA format for both. I also attached a discussion grading rubric thats required for the class. Use scholarly resources to support your post and follow all guidelines of the discussion rubric.


In the range of pulmonary disorders, pulmonary embolism (PE) falls into the pulmonary vascular disease category. Other disorders that are in this category are pulmonary hypertension and cor pulmonale.
Pulmonary embolism is the sudden blockage of a major blood vessel in the lung. Although the cause of the blockage is usually a blood clot, other less common culprits can be air bubbles (which may occur with certain scenarios in SCUBA diving), foreign bodies like needles or catheter tips, tissue fragments, tumors, and fat – such as when a major fracture occurs and releases fat into the blood system.
With blood clots being the most common cause of PE however, anything that promotes blood abnormal blood clotting sets one up for a higher risk for the development of a PE. And when the cause is a blood clot, the most common site of origin of the blood clot itself before it travels to the pulmonary vessels is the lower leg. Brashers & Heuther (2014, p. 1275) state:
Risk factors for PE include conditions and disorders that promote blood clotting as a result of venous stasis (immobilization, heart failure), hypercoagulability (inherited coagulation disorders, malignancy, hormone replacement, oral contraceptives, pregnancy), and endothelial injury to the cells that line the vessels (trauma, caustic intravenous infusions).
Other risks include genetic risk factors, among them factor V Leiden mutation, antithrombin II deficiency, protein S deficiency, and prothrombin 20210 gene mutations.
Söderberg, Brohult, Jorfeldt,& Lärfars (2009) find that the use of D-dimer testing has a reasonable reliability in ruling out PE. They state (p. ) “D-dimer testing has become a biochemical marker used widely to eliminate deep venous thrombosis and PE [i.e. venous thromboembolism (VTE)] from the list of diagnoses to consider, mainly in patients with a low risk of disease” (p. 129).


Brashars & Huether (2014, p. 1275) state that PE can cause any of the following four results. Embolus with infarction, embolus without infarction, massive occlusion, or multiple pulmonary emboli. Infarction is this context is the permanent loss of lung tissue in the area normally perfused by the affected blood supply. There is death of a portion of lung tissue.
In addition to the direct effect that the reduced blood supply causes to the lungs, there are additional, secondary effects that can be seen, as noted by Brashars & Huether (2014, p. 1275).
As a result of the thrombus lodging in the pulmonary circulation, there is a release both of neurohumoral substances, such as serotonin, histamine, catecholamines, and angiotensin II, and of inflammatory mediators, such as endothelin, leukotrienes, thromboxanes, and toxic oxygen free radicals. This causes widespread vasoconstriction that further impedes blood flow to the lung.
They go on to say that all of this can lead to right heart failure, atelectasis, hypoxemia, and that even death is possible depending upon the size of the blockage and how much lung is affected.

Clinical Manifestations

Brashars & Huether list “…the sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety” (p. 1276) as the typical presentation of PE. However, depending on the size of the occlusion, the symptoms may be as bad as “…profound shock, hypotension, tachypnea, tachycardia, severe pulmonary hypertension, and chest pain”.
If the underlying cause of the PE is deep venous thrombosis (DVT), the clinical manifestations of that precursor condition are calf pain and calf tenderness as well as calf asymmetry. However, Brashars and Huether caution that the absence of such recognizable signs and symptoms of DVT does not preclude the possibility of PE.

The best treatment for PE is prevention. In the inpatient hospital setting, this means getting patient up and moving around to prevent venous stasis. Even in the healthy population, those on long car rides or airplane flights can practice prevention by making sure to take periodic walking breaks. For patients and healthy individuals for whom walking is not an option, other options include the use of pneumatic compression stockings, leg exercises from bed or chair, hydration, and frequent position changes. Prevention in the population of predisposed individuals with clotting abnormalities is the recognition and treatment of these issues before PE has a chance to occur. Some individuals qualify for the placement of a filter in the inferior vena cava to stop emboli from entering the lungs, but these filters have to be surgically placed and removed and carry risks of their own.
For those in whom prevention either wasn’t carried out, or failed to work, treatment consists largely of anticoagulation medications to dissolve clots and/or to keep new clots from forming. These measure are of course for stable patients. Unstable patients may need both anticoagulation therapy and supportive measures such as supplemental oxyen, or even surgery to remove the clot(s).
One such drug treatment is heparin. “Heparin, the primary pharmacologic agent, does not dissolve clots but prevents formation of further thrombi by inhibiting thrombin and activated clotting factors II, IX, X, XI, and XII and also by utilizing and potentiating antithrombin III” “Dilucent, 2001, p. 57). However, drugs such as actual clot busters (thrombolytic agents) are streptokinase, urokinase, and tissue plasminogen activator. These drugs carry their own set of risks from hemorrhage and stroke but have several advantages, chied among them rapid clot dissolution.

Brashars, V. L., & Huether, S. E. (2014). Alterations of pulmonary function. In K. McCance & S. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 527-580). St Louis, MO: Elsevier Mosby.
DiLucente, M. (2001). Pulmonary embolism: a nursing perspective. Topics In Emergency Medicine, 23(1), 53-60.
Söderberg, M., Brohult, J., Jorfeldt, L., & Lärfars, G. (2009). The use of D-dimer testing and Wells score in patients with high probability for acute pulmonary embolism. Journal Of Evaluation In Clinical Practice, 15(1), 129-133.



Chronic obstructive pulmonary disease (COPD) is an increasingly common, the third leading cause of death in the US, and often preventable and treatable (American Lung Association, 2016). In the United States, the term “COPD” includes two main conditions—emphysema, and chronic bronchitis, and the leading cause of COPD is cigarette smoking (NIH, 2013a). Another environmental cause is exposure to biomass fuels such as cooking on oil, wood or coal burning stoves in enclosed spaces (Holmes and Murdoch, 2016). There are also genetic factors that can cause COPD which according to Casey (2016), “There is an identified association in rates of COPD between family members (regardless of tobacco exposure), which indicates underlying genetic influences. A very small number of people with emphysema have a hereditary defect in the genes responsible for producing alpha-1-antitrypsin and this was the first genetic association with COPD to be determined. More recently, a number of genes involved in regulating enzyme activity and receptor function have been linked to COPD, but none conclusively” (p. 21). Irritants cause inflammation and eventually edema and the number and size of mucous glands. Impairment of ability to clear mucous leads to susceptibility of pulmonary infection (McCance and Huether, 2014).

Clinical manifestations of COPD productive cough, decreased exercise tolerance, wheezing, and shortness of breath (McCance and Huether, 2014). According to Holmes and Murdoch (2016) common co-morbidities associated with COPD are: Coronary heart disease, heart failure, diabetes, erectile dysfunction, osteoporosis, incontinence, and anxiety. Treatment for COPD is varied and depends on stages of the disease. Treatments can include: bronchodilators, bronchodilators with glucocorticosteroids, flu and pneumonia vaccines, pulmonary rehabilitation, oxygen therapy, surgery, bullectomy, lung volume reduction surgery, and lung transplant (NIH, 2013b). The number one lifestyle change for patients with COPD would be to quit smoking. Education on smoke cessation groups and treatments are easily available online.


American Lung Association. (2016). COPD. Retrieved from:

Casey, G. (2016). COPD: obstructed lungs. Kai Tiaki Nursing New Zealand, 22(5), 20-24. Retrieved from:

Holmes, S., & Murdoch, C. (2016). Advances in COPD: a glimpse of the future. Practice Nurse, 46(4), 34-40. Retrieved from:

McCance, K. L., & Huether, S. E. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed. Chapter 35). St Louis, MO: Elsevier Mosby

National Institute of Health (NIH). (2013a). What is COPD? Retrieved from:

National Institute of Health (NIH). (2013b). How is COPD treated? Retrieved from:

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