Pathophysiology Case Studies
As a student nurse practitioner working within a medical assessment ward, I deal with a wide variety of patients who present with both acute and chronic conditions.
This case study will identify the pathophysiology; look at the manifestations and clinical features of a condition. It will also discuss the therapeutic interventions and in turn evaluate the effectiveness of the interventions applied.
Kyna (a pseudonym) was a forty-nine year old lady who was admitted to the ward for further investigations for a suspected deep vein thrombosis. She had never been in hospital before and had no medical or surgical history other than the fact that she was clinically obese, with a body mass index of 32, and had been attending her GP for hormone replacement …show more content…
Furthermore, low pressures within the system complicate the haemodynamics. When a person stands upright, the hydrostatic pressure exceeds dynamic pressure impeding venous return. The action of the calf muscle pump overcomes this, which in turn can return the blood to the heart (Hirsch 1994). Laminar flow is also interfered with by clot formation. This promotes thrombus formation by bringing platelets into contact with the endothelium. Endothelial injury to blood vessels from a variety of sources is the most common cause of thrombus formation as stated by Cotran et al 1999. Porth 2005 goes on to explain that the endothelial layer provides a smooth and slippery inner surface for the vessel, which prevents platelet adherence and blood clotting as long as it remains intact. The endothelial cells produce prostacyclin, which produces a number of vasoconstrictor substances; plasmin and endothelium derived relaxing factors, all of which are important inhibitors of intravascular coagulation. A venous catheter can be used as an example of a source of vascular injury where the endothelial lining is disrupted, resulting in increased fibrin strands gathering at the site of injury, allowing a clot to …show more content…
British Journal of Surgeons , 86: 992-1004.
Anand SS, Wells Ps, Hunt D, Brill-Edards P, Cook D, Ginsberg JS (1998) Does this patient have deep vein thrombosis? JAMA, 279 (14):1094-1099.
Anderson DR (1999),Thrombosis in the emergency department, Arch Intern Med 159:477.
Aquila A (2001), “Deep venous Thrombosis,” Journal of Cardiovascular Nursing. 15(4):25-44.
Bounameaux H, de Moerloose P, Perrier A, Reber G (Jan 1994), Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: An overview. Thrombosis Haemostatsis. 71(1): 1-6.
Cotran RS (1999): Robbins’ pathologic basis of disease, ed 6, Philadelphia, W.B. Saunders.
Crowther MA, Harrison L, Hirsh J. Reply(1999), Warfarin: less may be better. Annual International Medical Journal : 127:333.
Daly E, Vessey MP, Hawkins MM, Carson JL, Gough P, Marsh S (1996), Risk of venous thromboembolism in users of hormone replacement therapy. Lancet; 346: 977-980.
Department of Health. Advice on travel-related deep vein thrombosis. URL: http://www.doh.gov.uk/dvt. (accessed on
This case study will identify the pathophysiology; look at the manifestations and clinical features of a condition. It will also discuss the therapeutic interventions and in turn evaluate the effectiveness of the interventions applied.
Kyna (a pseudonym) was a forty-nine year old lady who was admitted to the ward for further investigations for a suspected deep vein thrombosis. She had never been in hospital before and had no medical or surgical history other than the fact that she was clinically obese, with a body mass index of 32, and had been attending her GP for hormone replacement …show more content…
Furthermore, low pressures within the system complicate the haemodynamics. When a person stands upright, the hydrostatic pressure exceeds dynamic pressure impeding venous return. The action of the calf muscle pump overcomes this, which in turn can return the blood to the heart (Hirsch 1994). Laminar flow is also interfered with by clot formation. This promotes thrombus formation by bringing platelets into contact with the endothelium. Endothelial injury to blood vessels from a variety of sources is the most common cause of thrombus formation as stated by Cotran et al 1999. Porth 2005 goes on to explain that the endothelial layer provides a smooth and slippery inner surface for the vessel, which prevents platelet adherence and blood clotting as long as it remains intact. The endothelial cells produce prostacyclin, which produces a number of vasoconstrictor substances; plasmin and endothelium derived relaxing factors, all of which are important inhibitors of intravascular coagulation. A venous catheter can be used as an example of a source of vascular injury where the endothelial lining is disrupted, resulting in increased fibrin strands gathering at the site of injury, allowing a clot to …show more content…
British Journal of Surgeons , 86: 992-1004.
Anand SS, Wells Ps, Hunt D, Brill-Edards P, Cook D, Ginsberg JS (1998) Does this patient have deep vein thrombosis? JAMA, 279 (14):1094-1099.
Anderson DR (1999),Thrombosis in the emergency department, Arch Intern Med 159:477.
Aquila A (2001), “Deep venous Thrombosis,” Journal of Cardiovascular Nursing. 15(4):25-44.
Bounameaux H, de Moerloose P, Perrier A, Reber G (Jan 1994), Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: An overview. Thrombosis Haemostatsis. 71(1): 1-6.
Cotran RS (1999): Robbins’ pathologic basis of disease, ed 6, Philadelphia, W.B. Saunders.
Crowther MA, Harrison L, Hirsh J. Reply(1999), Warfarin: less may be better. Annual International Medical Journal : 127:333.
Daly E, Vessey MP, Hawkins MM, Carson JL, Gough P, Marsh S (1996), Risk of venous thromboembolism in users of hormone replacement therapy. Lancet; 346: 977-980.
Department of Health. Advice on travel-related deep vein thrombosis. URL: http://www.doh.gov.uk/dvt. (accessed on