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USW1.46926.202030 - NURS-6501N-47,Advanced Pathophysiology.2019 Winter Qtr 11/25-02/16-PT27

Assignment - Week 4

semiloore Akerele on Mon, Dec 23 2019, 2:50 AM 60% highest match Submission ID: 51f66acd-31c4-44cf-97bc-e15b2de0a79f

• wk4assgn Akerele S Patho.docx

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Running head: 1 DISORDERS OF THE VEINS AND ARTERIES 1 Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx DISORDERS OF THE VEINS AND ARTERIES 1 Source - Another student's paper DISORDERS OF THE VEINS AND ARTERIES 1 2 DISORDERS OF THE VEINS AND ARTERIES 6 Suspected Entry: 84% match Uploaded - wk4assgn Akerele S Patho.docx DISORDERS OF THE VEINS AND ARTERIES 6 Source - Another student's paper Disorders of the Veins and Arteries Disorders of the Veins and Arteries Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Disorders of the Veins and Arteries Source - Another student's paper Disorders of the Veins and Arteries Semiloore Akerele Walden University: NURS- 6501N December 22nd , 2019. 3 Disorder of the Veins and Arteries Two of the most common medical disease in adult population are Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) that presents so many similarities. Suspected Entry: 76% match Uploaded - wk4assgn Akerele S Patho.docx Disorder of the Veins and Arteries Two of the most common medical disease in adult population are Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) that presents so many similarities Source - Another student's paper Disorder of the Veins and Arteries Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) are two prevalent disorders that present with many similarities It is imperative as an advanced nurse practitioner to have a knowledge of the differences between these two disorders as well as their differences to prevent misdiagnosis. mistreatments, and possible complications that might arise during the course of the treatment of the disease. This paper is aimed at identifying the pathophysiology of CVI and DVT, difference between CVI and arterial thrombosis. 3 Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses Source - Another student's paper Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses Also, a constructed mind map will accentuate the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis. Suspected Entry: 90% match Uploaded - wk4assgn Akerele S Patho.docx Also, a constructed mind map will accentuate the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis Source - Another student's paper Lastly, a constructed mind map will highlight the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis Pathophysiology of Chronic Venous Insufficiency According to Heuther and McCance (2017), Varicose vein and valvular insufficiency can progress to Chronic Venous Insufficiency (CVI). CVI is an inadequate venous return over a period of time which result in pool of blood within the vein which results into swollen, twisted and tangible vein. 4 Structurally, the veins are thin walled highly distensible vessels with valves to prevent backflow and pooling of blood. Suspected Entry: 78% match Uploaded - wk4assgn Akerele S Patho.docx Structurally, the veins are thin walled highly distensible vessels with valves to prevent backflow and pooling of blood Source - Another student's paper Huether & McCance (2017) defines veins as “thin-walled, highly distensible vessels with valves to prevent backflow and pooling of blood” (p When one valve is damaged and there is an inadequate venous return, section of the vein is subjected to the pressure of a larger volume of blood under the influence of gravity which result int swelling of the surrounding tissue (Heuther & McCance, 2017). 2 Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues Source - Another student's paper Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues This process induces a fibrosclerotic remodeling of the skin which then causes ulceration. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx This process induces a fibrosclerotic remodeling of the skin which then causes ulceration Source - Another student's paper This process induces a fibrosclerotic remodeling of the skin which then causes ulceration (Huether & McCance, 2017). Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx (Huether & McCance, 2017) Source - Another student's paper (Huether & McCance, 2017) 5 Pathophysiology of Deep Vein Thrombosis Deep Vein Thrombosis (DVT) essentially occurs in the lower extremities. Suspected Entry: 80% match Uploaded - wk4assgn Akerele S Patho.docx Pathophysiology of Deep Vein Thrombosis Deep Vein Thrombosis (DVT) essentially occurs in the lower extremities Source - Another student's paper Deep Vein Thrombosis Deep vein thrombosis (DVT) are clots that essentially occur in the lower extremities 6 Three factors are known to promote DVT (the triad of Virchow): Suspected Entry: 82% match Uploaded - wk4assgn Akerele S Patho.docx Three factors are known to promote DVT (the triad of Virchow) Source - Another student's paper Three factors promote DVT known as the Triad of Virchow which includes 2 venous stasis, venous injury, and hypercoagulable states. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx venous stasis, venous injury, and hypercoagulable states Source - Another student's paper venous stasis, venous injury, and hypercoagulable states DVT’s builds up when the inner lining the vessels are damaged/ impaired. 3 This impairment initiates the clotting cascade to heal the damaged epithelium. Suspected Entry: 74% match Uploaded - wk4assgn Akerele S Patho.docx This impairment initiates the clotting cascade to heal the damaged epithelium Source - Another student's paper This damage initiates the clotting cascade to heal the injured epithelium 6 The accumulation of clotting factors and platelets lead to thrombus formation which usually occur at the venous valve. Suspected Entry: 71% match Uploaded - wk4assgn Akerele S Patho.docx The accumulation of clotting factors and platelets lead to thrombus formation which usually occur at the venous valve Source - Another student's paper Accumulation of clotting factors and platelets leads to thrombus formation in the vein, often near a venous valve The growth of the thrombus leads to increase in blood pressure while blood flow diminishes. 2 Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency Source - Another student's paper Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency DVT can lead to a clot breaking off and go to the lungs which is called pulmonary embolism and can also result in embolic stroke or death. 2 (Hammer & McPhee, 2014). Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx (Hammer & McPhee, 2014) Source - Another student's paper (Hammer & McPhee, 2014) 7 Differences between venous thrombosis and arterial thrombosis A thrombus can develop in either the arterial system or the venous system. Suspected Entry: 83% match Uploaded - wk4assgn Akerele S Patho.docx Differences between venous thrombosis and arterial thrombosis A thrombus can develop in either the arterial system or the venous system Source - Another student's paper The Differences between Venous Thrombosis and Arterial Thrombosis A thrombus is composed of fibrin and blood cells and can develop in either the arterial or the venous system 8 The arterial thrombi form under the condition of high blood flow and rare composed mostly of platelet aggregates held together by fibrin stands. Suspected Entry: 82% match Uploaded - wk4assgn Akerele S Patho.docx The arterial thrombi form under the condition of high blood flow and rare composed mostly of platelet aggregates held together by fibrin stands Source - Another student's paper Arterial thrombi form under conditions of high blood flow and are composed mostly of platelet aggregates held together by fibrin stands(Huether & McCance,2017) 9 Venous thrombi form under the conditions of low blood flow and are composed of red cells with larger amounts of fibrin and few (Heuther & McCance 2017). Suspected Entry: 87% match Uploaded - wk4assgn Akerele S Patho.docx Venous thrombi form under the conditions of low blood flow and are composed of red cells with larger amounts of fibrin and few (Heuther & McCance 2017) Source - Another student's paper Venous thrombi form under conditions of low flow and are composed mostly of red cells with larger amounts of fibrin and few platelets (Huether & McCance, 2017) 10 Inflammation plays major role in the development of venous thrombosis while arterial thrombosis is influenced by the state of the coagulation system. Suspected Entry: 78% match Uploaded - wk4assgn Akerele S Patho.docx Inflammation plays major role in the development of venous thrombosis while arterial thrombosis is influenced by the state of the coagulation system Source - http://www.einthovenlaboratory.com/onderzoeken/the-link-between-venous-thrombosis-and-arterial-thrombosis/ Increasing evidence indicates that inflammation does also play a role in the development of venous thrombosis, while arterial thrombosis is influenced by the state of the coagulation system Venous thrombotic risk is determined by flexible combination of both acquired and genetic risk factor while arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking et.c. Suspected Entry: 66% match Uploaded - wk4assgn Akerele S Patho.docx Venous thrombotic risk is determined by flexible combination of both acquired and genetic risk factor while arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking et.c Source - http://www.einthovenlaboratory.com/onderzoeken/the-link-between-venous-thrombosis-and-arterial-thrombosis/ Arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking, unfavorable lipid profile et cetera ( Rosendale, 2016). Patient Factors: Gender (Female) Both male and female are affected by DVT and CVI, but female is at higher risk because of the possibility of pregnancy and also birth control. Rosendale (216), stated that, many drugs put the women at risk of developing thrombus which are basically female hormones and oral contraceptives (Rosendaal, 2016). Also, women between the age of 16 and 50 who are pregnant or on birth control are at risk of CVI and DVT. Countrywide according to Goldman & Weiss (2016), about 15% and 25% of women and men respectively are affected by varicose veins, and an approximated 3% estimated to affect European countries populations, prevalence compared to that of diabetes (Goldman & Weiss, 2016). CVI and DVT can be diagnosed by physical examination. D- timers is also done before proceeding to other diagnosis method. Ultrasonography diagnosis can also be done together with Doppler flow studies. D- timers are avoided in pregnant women because their serum D-timers is four times the normal value.in pregnant women. For DVT is treated using injectable with anticoagulant heparin followed by oral anticoagulant (Baker & dela Cruz, 2019). For pregnant women, low molecular weight heparin is usually recommended. They are also encouraged to stay active and wearing of compression stocking. Comment by Semiloore Akerele: Comment by Semiloore Akerele: To exclude DVT, Ultrasonography diagnosis is specifically done with clinical testing for CVI. CVI’s treatment depends on the disorder's severity and a patient should follow a dietary sodium and lifestyle changes, pneumatic devices, surgery, topical wound care and compression using bandages (Gujja, Sanina & Wiley, 2017). 3 Conclusion The pathophysiology, similarities and differences of these diseases have been discussed, and the pathology has been considered with the patient factor of female in mind. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Conclusion The pathophysiology, similarities and differences of these diseases have been discussed, and the pathology has been considered with the patient factor of female in mind Source - Another student's paper Conclusion The pathophysiology, similarities and differences of these diseases have been discussed, and the pathology has been considered with the patient factor of female in mind MAP MIND DVT mind mapDIAGNOSIS Ultrasound D-dimer History Physical examination CLINICAL PRESENTATION Pain Holman’s sign Extremity redness Redness TREATMENT Heparin Elevation of legs Compression stockings Warfarin 11 DEEP VENOUS THROMBOSIS Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx DEEP VENOUS THROMBOSIS Source - https://papyrus.bib.umontreal.ca/xmlui/handle/1866/5464 deep venous thrombosis EPIDEMIOLOGY Slowed venous blood flow Biochemical imbalance between circulating factors 12 PATHOPHYSIOLOGY Venous stasis Suspected Entry: 63% match Uploaded - wk4assgn Akerele S Patho.docx PATHOPHYSIOLOGY Venous stasis Source - https://coggle.it/diagram/WNP1ok0gXwABrEbg/t/- Venous stasis ulcer Obstruction of blood flow Vessel damage Hypercoagulability CVI mind mapDIAGNOSIS Vascular ultrasound Pulses that are non-palpable are determined by Doppler studies Using history and physical examination Lower extremities carefully inspected and palpated. TREATMENT Non-invasive treatment: Compression stockings Physical exercise Lower extremities are elevated Invasive treatment: 13 Sclerotherapy or surgical Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Sclerotherapy or surgical Source - Another student's paper Sclerotherapy or Surgical Ligation Vein resection Vein stripping 2 CHRONIC VENOUS INSUFFICIENCY Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx CHRONIC VENOUS INSUFFICIENCY Source - Another student's paper Chronic Venous Insufficiency EPIDEMIOLOGY Valve damage Reduced mobility Shock Advanced age Stasis ulcers 1 Dry, rough skin Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Dry, rough skin Source - Another student's paper Dry,!rough!skin PATHOPHYSIOLOGY Inadequate supply of oxygen rich-blood leads to necrosis development Damaged vales and venous walls inhibiting their function Blood clot in lower extremities due to damaged valves Weakened walls and valves cause insufficient venous return impairing blood flowing to the heart. CLINICAL PRESENTATION Rough and dry skin Stasis ulcers Hyperpigmentation Swollen lower extremity Patients complain of leg pains and feeling tired quickly References Baker, M., & dela Cruz, J. (2019). 11 Deep Venous Thrombosis Ultrasound Evaluation. Suspected Entry: 71% match Uploaded - wk4assgn Akerele S Patho.docx Deep Venous Thrombosis Ultrasound Evaluation Source - https://papyrus.bib.umontreal.ca/xmlui/handle/1866/5464 deep venous thrombosis 6 Dresang L.T., Fontaine P., Leeman L., King V. Suspected Entry: 94% match Uploaded - wk4assgn Akerele S Patho.docx Dresang L.T., Fontaine P., Leeman L., King V Source - Another student's paper Dresang, L.T., Fontaine, P., Leeman, L., & King, V.J J. 2 (2008).Venous Thromboembolism During Pregnancy. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx (2008).Venous Thromboembolism During Pregnancy Source - Another student's paper (2008).Venous Thromboembolism During Pregnancy Am Fam Physician,15;77(12):1709-1716. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Am Fam Physician,15;77(12):1709-1716 Source - Another student's paper Am Fam Physician,15;77(12):1709-1716 https://www.aafp.org/afp/2008/0615/p1709.html#sec-5 Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx https://www.aafp.org/afp/2008/0615/p1709.html#sec-5 Source - Another student's paper https://www.aafp.org/afp/2008/0615/p1709.html#sec-5 Goldman, M. P., & Weiss, R. A. (2016). Sclerotherapy E-book: 7 Treatment of Varicose and Telangiectatic Leg Veins. Suspected Entry: 64% match Uploaded - wk4assgn Akerele S Patho.docx Treatment of Varicose and Telangiectatic Leg Veins Source - Another student's paper Treatment for Varicose Veins 14 Elsevier Health Sciences. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Elsevier Health Sciences Source - Another student's paper Elsevier Health Sciences Gujja, K., Sanina, C., & Wiley, J. M. (2017). 2 Chronic venous insufficiency. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Chronic venous insufficiency Source - Another student's paper Chronic Venous Insufficiency Interventional Cardiology: Principles and Practice, 759-767. Hammer, G. G. , & McPhee, S. (2014). 2 Pathophysiology of disease: Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Pathophysiology of disease Source - Another student's paper Pathophysiology of disease An introduction to clinical medicine. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx An introduction to clinical medicine Source - Another student's paper An introduction to clinical medicine (7th ed.) New York, NY: Suspected Entry: 99% match Uploaded - wk4assgn Akerele S Patho.docx (7th ed.) New York, NY Source - Another student's paper (7th ed.) New York, NY McGraw-Hill Education. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx McGraw-Hill Education Source - Another student's paper McGraw-Hill Education Huether, S. 2 E., & McCance, K. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx E., & McCance, K Source - Another student's paper E., & McCance, K L. (2017). 2 Understanding pathophysiology (6th ed.). Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Understanding pathophysiology (6th ed.) Source - Another student's paper Understanding pathophysiology (6th ed.) St. Louis, MO: Mosby. Rosendaal, F. R. (2016). 2 Causes of venous thrombosis. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Causes of venous thrombosis Source - Another student's paper Causes of venous thrombosis Thrombosis Journal, 14(Suppl 1), 24. Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx Thrombosis Journal, 14(Suppl 1), 24 Source - Another student's paper Thrombosis Journal, 14(Suppl 1), 24 http://doi.org/10.1186/s12959-016-0108-y Suspected Entry: 100% match Uploaded - wk4assgn Akerele S Patho.docx http://doi.org/10.1186/s12959-016-0108-y Source - Another student's paper http://doi.org/10.1186/s12959-016-0108-y