course material

1. Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).Review the section
“Diseases of the Veins” (pp. 598-599) in Chapter 23 of the Huether and McCance text.
Identify the pathophysiology of chronic venous insufficiency and deep venous thrombosis.
Consider the similarities and differences between these disorders.Select a patient factor
different from the one you selected in this week’s Discussion: genetics, gender, ethnicity,
age, or behavior. Think about how the factor you selected might impact the pathophysiology
of CVI and DVT.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
Reflect on how you would diagnose and prescribe treatment of these disorders for a patient
based on the factor you selected.ORDER A PLAGIARISM-FREE PAPER HEREReview the
“Mind Maps—Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD)”
media in the Week 2 Learning Resources. Use the examples in the media as a guide to
constructing two mind maps—one for chronic venous insufficiency and one for venous
thrombosis. Consider the epidemiology and clinical presentDeep Venous Thrombosis (DVT)
and Chronic Venous Insufficiency (CVI).ation of both chronic venous insufficiency and deep
venous thrombosis.To Complete:>>>Write a 2- to 3-page paper that addresses the
following:Compare the pathophysiology of chronic venous insufficiency and deep venous
thrombosis. Describe how venous thrombosis is different from arterial thrombosis.Explain
how the patient factor you selected might impact the pathophysiology of CVI and DVT.
Describe how you would diagnose and prescribe the treatment of these disorders for a
patient based on the factor you selected.Construct two mind maps—one for chronic venous
insufficiency and one for deep venous thrombosis. Include the epidemiology,
pathophysiology, and clinical presentation, as well as the diagnosis and treatment you
explained in your paper.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency
(CVI).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI):
Epidemiology, Pathophysiology, Clinical Presentation, Diagnosis, and ManagementDeep
venous thrombosis (DVT) and chronic venous insufficiency (CVI) are two vascular
conditions that are related. CVI causes stasis of blood in the deep veins of the extremities.
This stasis thereafter may lead to formation of a clot hence thrombosis in the deep vein.
This clot from the DVT may then dislodge and cause pulmonary embolism, a life-threatening
medical emergency.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency
(CVI).PathophysiologySince the two are related as indicated above, their pathophysiology is
also tied to one another. In CVI, valvular incompetence, venous hypertension (due to the
pooling of blood), and vessel wall inflammation interact to produce symptoms of venous

2. insufficiency. In immobile patients and those with cardiac disease, the process above is
speeded up by improper functioning of the muscle pump and the heart (vascular pump)
respectively. The pooling of blood on the deep veins result in venous hypertension. Coupled
with the hemodynamic changes that ensue, the release of various vasoactive chemicals is
initiated. Subsequently, chemokines, adhesion molecules, and other mediators of
inflammation are produced. The end result endothelial injury (Huether & McCance, 2017;
Santler & Goerge, 2017; Hammer & McPhee, 2014).As for DVT, the pathophysiology is tied
to impaired venous return (venous stasis) and malfunctioning of either or both the muscle
pump and the vascular pump (the heart). As stated above, stasis can occur due to CVI hence
the relationship between the two. As such, injury to the vascular endothelium of the deep
veins in the extremities results in inflammation. At times, this injury may be the result of
invasive medical procedures such as insertion of a central venous catheter. Coupled with
hypercoagulability of the blood, the result is development of thrombi in the deep leg, arm,
or pelvic veins. This is DVT (Huether & McCance, 2017; Santler & Goerge, 2017; Hammer &
McPhee, 2014).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency
(CVI).Venous Thrombosis vs Arterial ThrombosisVenous thrombosis occurs in the nlood
vessels that return blood to the heart. Basically, a clot forms in one of the deep veins usually
due to hypercoagulability and injury to the venous endothelium. The thromboembolism
from this usually leads to pulmonary embolism. Arterial thrombosis on the other hand
involves clot formation in the vessels carrying oxygenated blood from the heart. Unlike in
venous thrombosis, the cause here is usually the formation of an atheromatous or fatty
plaque in the arterial wall. This progressively narrows the arterial lumen increasing the
velocity of blood passing at that particular point. The increased friction causes damage to
the arterial endothelium and a clot begons to form. This may finally dislodge and cause a
myocardial infarction or heart attack (if it is on the coronary arteries), or a stroke (if it is in
the brain) (Huether & McCance, 2017; Santler & Goerge, 2017; Hammer & McPhee,
2014).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).The Obesity
FactorObesity as a patient predisposing factor plays a very important role in the
pathophysiology of both CVI and DVT. For a start, it has been explained above that immobile
or physically inactive persons are at greater risk of developing CVI and DVT. This is because
the action of the muscle pump in aiding venous return will be absent. It is a fact that persons
who are obese loathe walking or just engaging in any phusical activity. The other reason is
that the heart of an obese person is overburdened. Its efficiency as a vascular pump is
significantly reduced due to the increased body mass and lack of exercise. This encourages
venous stasis (Huether & McCance, 2017; Hammer & McPhee, 2014).Epidemiology, Clinical
Presentation, Diagnosis, and TreatmentThe average prevalence of CVI has been put at 1 in 4
people in the general population. There is however considerable variability in the figures
for males and for females. Age, obesity, and a family history are significant risk factors. For
DVT, about 200,000 persons develop the condition annually, with the incidence standing at
80 diagnoses per 100,000 (Huether & McCance, 2017; Hammer & McPhee, 2014). The
clinical presentation of CVI includes night leg cramps, itchiness of the legs, edema and a
feeling of heaviness in the legs. Untreated, huge varicose veins greater than 3mm in
diameter become visible to the naked eye. As for DVT, symptoms include calf tenderness,

3. edema, and swelling of the whole extremity (Huether & McCance, 2017)..Deep Venous
Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).Diagnosis of CVI is basically done
based not only on imaging tests, but also on the history and clinical presentation. The
imaging studies include duplex ultrasonography and phlebography (contrast-enhanced X-
ray of the affected veins). For DVT, the rule of thumb is to use doppler ultrasonography for
diagnosis (Huether & McCance, 2017; Hammer & McPhee, 2014). Treatment of both CVI and
DVT can be either conservative or invasive, depending on the stage and the severity of
symptoms. For uncomplicated CVI, physical therapy in addition to manual compression
therapy is the standard. If severe, surgery to remove the incompetent vein or isolate the
source of stasis is the last option. For DVT, treatment is by anticoagulants. Surgery may
however be the next option in the case of recalcitrant thrombi (Huether & McCance, 2017;
Santler & Goerge, 2017).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency
(CVI).