Disorder of the Veins and Arteries Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) are two prevalent disorders that present with many similarities. Understanding the differences between these two similar but very different disorders can prevent needless misdiagnoses, unnecessary treatments, and complications in the treatment of the disease.The Purpose of this paper is to identify the pathophysiology of Chronic Venous Insufficiency and Deep Vein Thrombosis and their similarities and differences. Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses. 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 Chronic Venous Insufficiency (CVI) begins with the development of varicose veins in the deep veins. Varicose Veins are veins in which blood have pooled, and this pooling of blood causes swollen, twisted and tangible veins. Usually, veins are structures that have thin stretchable walls with valves used to prevent backflow and pooling of blood in the veins. Because the veins are structures used to bring blood back to the heart, gravity and valve malfunction over time can cause a varicose vein. When blood pooling occurs, the gravity in the veins causes the surrounding tissue to become swollen. Varicose veins can develop into CVI when there is an inadequate venous return over an extended period. 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. (Huether & McCance, 2017). Pathophysiology of Deep Vein Thrombosis Deep Vein Thrombosis (DVT) is caused by three factors (the triad of Virchow): venous stasis, venous injury, and hypercoagulable states. DVT’s begins to form when damage occurs to the inner lining of the vessel wall. This damage initiates the clotting cascade to heal the injured epithelium. As the thrombus grows blood pressure increase and blood flow decreases; Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency. Complications of DVT include pulmonary embolism and embolic stroke. (Hammer & McPhee, 2014). Similarities and Differences between the Disorders The similarity in the risk factors between these two illnesses includes an increase in age, the female gender, pregnancy, a leg injury, and obesity. Differences in the risk factors are that DVT can be a risk factor for CVI, but CVI cannot cause a DVT. To my understanding, everything that causes DVT can potentially can CVI since DVT is a risk fact ...

1. Disorder of the Veins and Arteries
Chronic Venous Insufficiency (CVI) and Deep Vein
Thrombosis (DVT) are two prevalent disorders that present with
many similarities. Understanding the differences between these
two similar but very different disorders can prevent needless
misdiagnoses, unnecessary treatments, and complications in the
treatment of the disease.The Purpose of this paper is to identify
the pathophysiology of Chronic Venous Insufficiency and Deep
Vein Thrombosis and their similarities and differences. Also,
the patient factor followed will highlight the effects of the
female gender on the pathophysiology of these illnesses. 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
Chronic Venous Insufficiency (CVI) begins with the
development of varicose veins in the deep veins. Varicose Veins
are veins in which blood have pooled, and this pooling of blood
causes swollen, twisted and tangible veins. Usually, veins are
structures that have thin stretchable walls with valves used to
prevent backflow and pooling of blood in the veins. Because the
veins are structures used to bring blood back to the heart,
gravity and valve malfunction over time can cause a varicose
vein. When blood pooling occurs, the gravity in the veins
causes the surrounding tissue to become swollen. Varicose veins
can develop into CVI when there is an inadequate venous return
over an extended period. 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. (Huether &
McCance, 2017).

2. Pathophysiology of Deep Vein Thrombosis
Deep Vein Thrombosis (DVT) is caused by three factors
(the triad of Virchow): venous stasis, venous injury, and
hypercoagulable states. DVT’s begins to form when damage
occurs to the inner lining of the vessel wall. This damage
initiates the clotting cascade to heal the injured epithelium. As
the thrombus grows blood pressure increase and blood flow
decreases; Increased pressure in the vein behind the clot may
produce edema in the extremity, and persistent venous
obstruction can lead to Chronic Venous Insufficiency.
Complications of DVT include pulmonary embolism and
embolic stroke. (Hammer & McPhee, 2014).
Similarities and Differences between the Disorders
The similarity in the risk factors between these two illnesses
includes an increase in age, the female gender, pregnancy, a leg
injury, and obesity. Differences in the risk factors are that DVT
can be a risk factor for CVI, but CVI cannot cause a DVT. To
my understanding, everything that causes DVT can potentially
can CVI since DVT is a risk factor for CVI. (Johns Hopkins
Medicine, n.d.). The epidemiology is different because CVI can
be caused by DVT and other separate entities such as valvular
dysfunction and gravity. A DVT is only caused by the triad of
Virchow. The signs and symptoms are similar in these two
diseases processes because a DVT can become CVI over an
extended period. However, at times a DVT can present with
redness or discoloration and tenderness in a particular location
instead of generalized hyperpigmentation like CVI. (Mayo
Clinic, 2017). The diagnostic process of these two illnesses is
similar in that they both are both diagnosed using an ultrasound
and a venogram. The difference is that for the DVT, diagnostics
can also include a computerized tomography (CT), magnetic
resonance imaging (MRI), and a D-dimer blood test. (Mayo
Clinic, 2017). Treatment similarities include moving around,
wearing compression stockings, quitting smoking and
exercising. Treatment differences include different medications
regimes. Complication similarities include venous stasis ulcers,

3. and complication differences include the pulmonary embolism
and embolic strokes that are specific to DVT.
Patient Factors: Gender (Female)
Hormones seem to be the only reason why women are at a
higher risk for developing chronic venous insufficiency and
DVT than men. Apparently there are many drugs that increase
the risk of developing a thrombus, many of which are female
hormone and oral contraceptives. (Rosendaal, 2016). The influx,
duration, and exit of hormones in a pregnant woman during
pregnancy cause this patient population to be more at risk of
developing a DVT and CVI. Also, with pregnancy come
hypervolemia; the increase of fluid volume in the same fluid
space can cause the venous hypertension and place pressure on
the valves in the vessels, which can cause CVI overtime if the
initial stages of the condition are not treated. Now when
diagnosing and treating these disorders in the female
population, the only changes that I would have to take would be
in the pregnant women population. For expecting mothers
recommended diagnoses for a suspected DVT is venous
compression ultrasonography and recommended treatment for
DVT in pregnant mothers are low molecular weight heparin
injections, staying active, and wearing compression stockings.
Usually d-dimer blood tests are avoided because during
pregnancy, a woman’s serum d-dimer is four to five times
higher than normal because of her pregnant state (Dresang,
Fontaine , Leeman , King, 2008). As for pregnant women that
have chronic venous insufficiency, the diagnosis and treatment
would be not different from the rest of the population.
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.
References
Dresang L.T., Fontaine P., Leeman L., King V. J.
(2008).Venous Thromboembolism During Pregnancy. Am Fam
Physician,15;77(12):1709-1716.

4. https://www.aafp.org/afp/2008/0615/p1709.html#sec-5
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of
disease: An introduction to clinical medicine. (7th ed.) New
York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding
pathophysiology (6th ed.). St. Louis, MO: Mosby.
Johns Hopkins Medicine (n.d.). Chronic Venous Insufficiency.
Retrieved
from https://www.hopkinsmedicine.org/healthlibrary/conditions/
cardiovascular_diseases/chronic_venous_insufficiency
Mayo Clinic (2017). Deep Vein Thrombosis. Retrieved
from https://www.mayoclinic.org/diseases-conditions/deep-
vein-thrombosis/symptoms-causes/syc-20352557
Rosendaal, F. R. (2016). Causes of venous
thrombosis. Thrombosis Journal, 14(Suppl 1), 24.
http://doi.org/10.1186/s12959-016-0108-y