Diseases of the veins can involve varicose veins, chronic venous insufficiency, deep vein thrombosis, and superior vena cava syndrome. Varicose veins and chronic venous insufficiency are caused by damaged valves that allow blood to pool in the veins under gravity, distending and damaging the veins over time. Deep vein thrombosis occurs when blood clots form in the deep veins, usually in the legs, which can lead to pulmonary embolism if pieces of the clot break off. Superior vena cava syndrome involves the occlusion of the superior vena cava by lung cancer or other causes in most cases.

1. Diseases of The Veins Summary
Diseases of The Veins SummaryORDER HERE FOR ORIGINAL, PLAGIARISM-FREE PAPERS
ON Diseases of The Veins SummaryAs a learner in Pathophysiology, it’s important to take
the information you are absorbing from your coursework and connect it to real life.
Throughout the semester you will be invited to make connections by locating, reviewing,
and summarizing current and relevant journal articles.Use the following link to learn how to
find and evaluate an online source: https://www.nia.nih.gov/health/online-health-
information-it-reliable#where (Links to an external site.)Please follow the instructions
below:1. Locate a current (medical or scientific) news or journal article based on one of the
topics listed below:Diseases of the Veins, (Chapter 24, p. 598)Note: As you read through the
article, think about how it connects to Pathophysiology and why is it relevant.2. Provide a
write-up summarizing the article. Within your document, include how the information
connects to Pathophysiology, and why it is relevant.3. Aim to include 150 – 200 words in the
summary.4. Remember to cite your source(s) in APA Format!Diseases of The Veins
Summaryattachment_1Unformatted Attachment PreviewUnderstanding Pathophysiology
FIRST CANADIAN EDITION Mohamed Toufic El-Hussein, RN, PhD Associate Professor,
School of Nursing Faculty of Health, Community & Education Mount Royal University
Calgary, Alberta Kelly Power-Kean, MHS, NP, RN Center for Nursing Studies Memorial
University St. John’s, Newfoundland Stephanie Zettel, BN, MN Associate Professor 2 School
of Nursing and Midwifery Mount Royal University Calgary, Alberta U.S. AUTHORS Sue E.
Huether, MS, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City,
Utah Kathryn L. McCance, MS, PhD Professor Emeritus College of Nursing University of Utah
Salt Lake City, Utah U.S. Section Editors Valentina L. Brashers, MD Professor of Nursing and
Woodard Clinical Scholar Attending Physician in Internal Medicine University of Virginia
Health System Charlottesville, Virginia Neal S. Rote, PhD Academic Vice-Chair and Director
of Research Department of Obstetrics and Gynecology University Hospitals Case Medical
Center William H. Weir, MD, Professor of Reproductive Biology and Pathology Case Western
Reserve University School of Medicine 3 Cleveland, Ohio 4 24 Alterations of Cardiovascular
Function Valentina L. Brashers, Mohamed El-Hussein CHAPTER OUTLINE Diseases of the
Veins, 604 Varicose Veins and Chronic Venous Insufficiency, 604 Thrombus Formation in
Veins, 605 Superior Vena Cava Syndrome, 605 Diseases of the Arteries, 606 Hypertension,
606 Orthostatic (Postural) Hypotension, 611 Aneurysm, 611 Thrombus Formation, 612
Embolism, 613 Peripheral Vascular Disease, 613 Atherosclerosis, 614 Peripheral Artery
Disease, 617 Coronary Artery Disease, Myocardial Ischemia, and 1791 Acute Coronary

2. Syndromes, 617 Disorders of the Heart Wall, 629 Disorders of the Pericardium, 629
Disorders of the Myocardium: The Cardiomyopathies, 630 Disorders of the Endocardium,
632 Cardiac Complications in AIDS, 638 Manifestations of Heart Disease, 638 Heart Failure,
638 Dysrhythmias, 643 Shock, 643 Impairment of Cellular Metabolism, 643 Clinical
Manifestations of Shock, 648 Treatment for Shock, 648 Types of Shock, 648 Multiple Organ
Dysfunction Syndrome, 653 Our understanding of the pathophysiology of cardiovascular
diseases is evolving rapidly. Neurohumoral, genetic, inflammatory, and metabolic factors
are now the focus. This new information is leading to improvements in prevention and
treatment. Diseases of the Veins 1792 Varicose Veins and Chronic Venous Insufficiency A
varicose vein is a vein in which blood has pooled, producing distended, tortuous, and
palpable vessels (Figure 24-1). Diseases of The Veins SummaryVeins are thin-walled, highly
distensible vessels with valves to prevent backflow and pooling of blood (see Figure 23-26).
Varicose veins typically involve the saphenous veins of the leg and are caused by (1) trauma
to the saphenous veins that damages one or more valves or (2) gradual venous distension
caused by the action of gravity on blood in the legs. FIGURE 24-1 Varicose Veins of the Leg.
(Solarisys/Shutterstock.com.) If a valve is damaged, a section of the vein is subjected to the
pressure of a larger volume of blood under the influence of gravity. Altered connective
tissue proteins and proteolytic enzyme activity also play a role in remodelling of the vessel
wall.1 The vein swells as it becomes engorged and surrounding tissue becomes edematous
because increased hydrostatic pressure pushes plasma through the stretched vessel wall.
Venous distension can develop over time in individuals who habitually stand for long
periods, wear constricting garments, or cross the legs at the knees, which 1793 diminishes
the action of the muscle pump (see Figure 23-27). Risk factors also include age, female
gender, a family history of varicose veins, obesity, pregnancy, deep venous thrombosis
(DVT), and previous leg injury. Eventually the pressure in the vein damages venous valves,
rendering them incompetent and unable to maintain normal venous pressure. Varicose
veins and valvular incompetence can progress to chronic venous insufficiency, especially in
obese individuals. Chronic venous insufficiency (CVI) is inadequate venous return over a
long period. Venous hypertension, circulatory stasis, and tissue hypoxia cause an
inflammatory reaction in vessels and tissue leading to fibrosclerotic remodelling of the skin
and then to ulceration. Symptoms include edema of the lower extremities and
hyperpigmentation of the skin of the feet and ankles. Edema in these areas may extend to
the knees. Circulation to the extremities can become so sluggish that the metabolic demands
of the cells to obtain oxygen and nutrients and to remove wastes are barely met. Any
trauma or pressure can therefore lower the oxygen supply and cause cell death and necrosis
(venous stasis ulcers) (Figure 24-2). Infection can occur because poor circulation impairs
the delivery of the cells and biochemicals necessary for the immune and inflammatory
responses. Diseases of The Veins SummaryThis same sluggish circulation makes infection
following reparative surgery a significant risk. FIGURE 24-2 Venous Stasis Ulcer. (From
Rosai, J. [1989]. Ackerman’s surgical pathology [7th ed., vol. 2]. St. Louis: Mosby.) Treatment
of varicose veins and CVI begins conservatively, and 1794 excellent wound healing results
have followed noninvasive treatments such as elevating the legs, wearing compression
stockings, and performing physical exercise.2 Invasive management includes endovenous

3. ablation, sclerotherapy or surgical ligation, conservative vein resection, and vein stripping.3
Thrombus Formation in Veins A thrombus is a blood clot that remains attached to a vessel
wall (see Figure 21-20). A detached thrombus is a thromboembolus. Venous thrombi are
more common than arterial thrombi because flow and pressure are lower in the veins than
in the arteries. Deep venous thrombosis (DVT) occurs primarily in the lower extremity.
Three factors (Virchow triad) promote venous thrombosis: (1) venous stasis (e.g.,
immobility, age, heart failure), (2) venous endothelial damage (e.g., trauma, intravenous
medications), and (3) hypercoagulable states (e.g., inherited disorders, malignancy,
pregnancy, use of oral contraceptives or hormone replacement therapy). Orthopedic trauma
or surgery, spinal cord injury, and obstetric/gynecological conditions can be associated
with up to a 100% likelihood of DVT. Numerous genetic abnormalities are associated with
an increased risk for venous thrombosis primarily related to states of hypercoagulability.
These inherited abnormalities include factor V Leiden mutation, prothrombin mutations,
and deficiencies of protein C, protein S, and antithrombin; these abnormalities are
commonly found in individuals who develop thrombi in the absence of the usual risk
factors.4 Accumulation of clotting factors and platelets leads to thrombus formation in the
vein, often near a venous valve. Inflammation around the thrombus promotes further
platelet aggregation, and the thrombus propagates or grows proximally. This inflammation
may cause pain and redness, but because the vein is deep in the leg, it is usually not
accompanied by clinical symptoms or signs. If the thrombus creates significant obstruction
to venous blood flow, increased pressure in the vein behind the clot may lead to edema of
the extremity. Most thrombi will eventually dissolve without treatment; however, untreated
DVT is associated with a high risk for embolization of a part of the clot to the lung
(pulmonary 1795 embolism) (see Chapter 27). Persistent venous obstruction may lead to
CVI and post-thrombotic syndrome with associated pain, edema, and ulceration of the
affected limb.5 Because DVT is usually asymptomatic and difficult to detect clinically,
prevention is important in at-risk individuals and includes early ambulation, pneumatic
devices, and prophylactic anticoagulation. If thrombosis does occur, diagnosis is confirmed
by a combination of serum D-dimer measurement and Doppler ultrasonography.
Management most often consists of anticoagulation therapy using heparin (low-molecular-
weight heparin) and warfarin (Coumadin).6 New oral anticoagulant therapies, such as
factor Xa inhibitors and direct thrombin inhibitors, have been shown to have a more
favourable benefit-torisk ratio and are rapidly becoming the treatments of choice.7
Thrombolytic therapy or placement of an inferior vena cava filter may be indicated in
selected individuals.4,6 Superior Vena Cava Syndrome Superior vena cava syndrome (SVCS)
is a progressive occlusion of the superior vena cava (SVC) that leads to venous distension in
the upper extremities and head. Causes include bronchogenic cancer (75% of cases)
followed by lymphomas and metastasis of other cancers.8 Other less common causes
include tuberculosis, mediastinal fibrosis, and cystic fibrosis. Invasive therapies (pacemaker
wires, central venous catheters, and pulmonary artery catheters) with associated
thrombosis now account for nearly 40% of cases.9 The SVC is a relatively low-pressure
vessel that lies in the closed thoracic compartment; therefore, tissue expansion can easily
compress the SVC. Diseases of The Veins SummaryThe right mainstem bronchus abuts the

4. SVC so that cancers occurring in this bronchus may exert pressure on the SVC. Additionally,
the SVC is surrounded by lymph nodes and lymph chains that commonly become involved
in thoracic cancers and compress the SVC during tumour growth. Because onset of SVCS is
most often slow, collateral venous drainage to the azygos vein usually has time to develop.
Clinical manifestations of SVCS are edema and venous distension in the upper extremities
and face, including the ocular beds. Affected persons complain of a feeling of fullness in the
head or 1796 tightness of shirt collars, necklaces, and rings. Cerebral edema may cause
headache, visual disturbance, and impaired consciousness. The skin of the face and arms
may become purple and taut, and capillary refill time is prolonged. Respiratory distress may
be present because of edema of bronchial structures or compression of the bronchus by a
carcinoma. In infants, SVCS can lead to hydrocephalus. Diagnosis is made by chest X-ray,
Doppler studies, computed tomography (CT), magnetic resonance imaging (MRI), and
ultrasound. Because of its slow onset and the development of collateral venous drainage,
SVCS is generally not a vascular emergency, but it is an oncological emergency. Treatment
for malignant disorders can include radiation therapy, surgery, chemotherapy, and the
administration of diuretics, steroids, and anticoagulants, as necessary. Treatment for
nonmalignant causes may include bypass surgery using various grafts, thrombolysis (both
locally and systemically), balloon angioplasty, and placement of intravascular stents.8 Quick
Check 24-1 1. What is chronic venous insufficiency, and how does it present clinically? 2.
What are the major risk factors for deep venous thrombosis? 3. Name three causes of
superior vena cava syndrome. Diseases of the Arteries Hypertension Hypertension is
consistent elevation of systemic arterial blood pressure.10 Approximately 7.5 million
Canadians have hypertension. Hypertension is considered to be the main factor
contributing to mortality, disability-adjusted life years (DALYs), and years of life lost (YLL)
in Canada. About 90% of Canadians are expected to develop hypertension if they live an
average lifespan.11 The chance of developing primary hypertension increases with 1797
age. Although hypertension is usually considered an adult health problem, it is important to
remember that hypertension does occur in children and is being diagnosed with increasing
frequency (see Chapter 25). The prevalence of hypertension is higher in those of African
descent and in those with diabetes. Hypertension is defined by Hypertension Canada as a
mean systolic blood pressure greater than or equal to 140 mm Hg or diastolic blood
pressure greater than or equal to 90 mm Hg when a nonautomated office blood pressure
measurement is used (Table 24-1). Alternately, hypertension is also defined as a mean
systolic blood pressure greater than or equal to 135 mm Hg or diastolic blood pressure
greater than or equal to 85 mm Hg when an automated office blood pressure measurement
is used.12 Diseases of The Veins SummaryFigure 24-3 presents a hypertension diagnostic
algorithm for adults. TABLE 24-1 Classification of Blood Pressure for Adults Age 18 Years
and Older Category Systolic (mm Hg) Normal Prehypertension Stage 1 hypertension Stage 2
hypertension <120 120–139 140–159 ≥160 Diastolic (mm Hg) AND OR OR OR <80 80–89
90–99 ≥100 Data from James, P.A., Oparil, S., Carter, B., et al. (2014). JAMA, 311(5), 507–
520. 1798 Hypertension Diagnostic Algorithm. 1If AOBP is used, use the mean calculated
and displayed by the device. If non-AOBP (see note 2) is used, take at least three readings,
discard the first, and calculate the mean of the remaining measurements. A history and

5. physical exam should be performed and diagnostic tests ordered. 2 AOBP is performed with
the patient unattended in a private area. NonAOBP is performed using an electronic upper
arm device with the provider in the room. 3Diagnostic thresholds for AOBP, ABPM, and
home BP in patients with diabetes have yet to be established (and might be lower than
13/80 mm Hg). 4Serial office measurements over 3–5 visits can be used if ABPM or home
measurement is not available. 5 For a home BP series, two readings are taken each morning
and evening for 7 days (28 total). Discard the first day readings and average the last 6 days.
6Annual BP measurement is recommended to detect progression to hypertension. ABPM,
ambulatory blood pressure measurement; AOBP, automated office blood pressure; BP,
blood pressure. (Reprinted from Can J Card, 33(5), Leung, A., Daskalopoulou, S.S., Dasgupta,
K., et al, FIGURE 24-3 “Hypertension Canada’s 2017 Guidelines for Diagnosis, Risk
Assessment, Prevention, and Treatment of Hypertension in Adults,” Pages 557–576,
Copyright 2017, with permission from Elsevier.) According to Hypertension Canada, all
Canadian adults should have their blood pressure checked each time they visit a clinic,
regardless of the reason. It is recommended that health care providers use automated
measurement of blood pressure rather than manual measurement. It is also recommended
that these measurements be done multiple times and be unattended. Patients are also
encouraged to record and report out-of-office blood 1799 pressure measurements to
confirm the initial diagnosis of hypertension. Optimum management of the hypertensive
patient requires thorough assessment and evaluation. Patients should be reminded that
modification of health behaviour is effective in preventing hypertension, treating
hypertension, and reducing cardiovascular risk. However, a combination of both health
behaviour changes and medications is often necessary to achieve target blood pressures.
Patients should be taught how to measure blood pressure at home to be involved in self-
monitoring and selfmanagement, and to promote adherence to medications and a healthy
diet.13 Normal blood pressure is associated with the lowest cardiovascular risk, whereas
those who fall into the prehypertension category are at risk of developing hypertension and
many associated cardiovascular complications unless lifestyle modification and treatment
are instituted. All stages of hypertension are associated with increased risk for target organ
disease events, such as myocardial infarction (MI), kidney disease, and stroke; thus both
stage I and stage II hypertension need effective long-term therapy. Most cases of
hypertension are diagnosed as primary hypertension (also called essential hypertension or
idiopathic hypertension). From 92 to 95% of hypertensive individuals have primary
disease. Secondary hypertension is caused by an underlying disorder such as renal disease.
This form of hypertension accounts for only 5 to 8% of cases. Factors Associated With
Primary Hypertension A specific cause of primary hypertension has not been identified, and
a combination of genetic and environmental factors is thought to be responsible for its
development. Genetic predisposition to hypertension is thought to be polygenic and
associated with epigenetic changes influenced by diet and lifestyle.14 Inherited defects are
associated with renal sodium excretion, insulin and insulin sensitivity, activity of the
sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS),
and cell membrane sodium or calcium transport.15 Diseases of The Veins SummaryFactors
associated with primary hypertension relate to age, gender, race, and dietary factors (see

6. Risk Factors: Primary Hypertension). Many of these factors are 1800 also risk factors for
other cardiovascular disorders. In fact, obesity, hypertension, dyslipidemia, and glucose
intolerance often are found together in a condition called metabolic syndrome (see Chapter
19). Risk Factors Primary Hypertension Family history Advancing age Cigarette smoking
Obesity Heavy alcohol consumption Gender (men greater than women before age 55;
women greater than men after 55) Being of African descent Being of Indigenous descent
Immigration-related change in socioeconomic status High dietary sodium intake Low
dietary intake of potassium, calcium, magnesium Glucose intolerance The Indigenous
population in Canada and primary hypertension. In Canada, the rate of developing and
dying of heart disease and stroke among Indigenous people is twice that in the rest of the
population. Moreover, Indigenous people are three to four times more likely to experience
type 2 diabetes mellitus than nonIndigenous people, and they are 10.5 times more likely to
die from coronary heart disease. About 40% of the Indigenous population in Canada lives on
reserves, thus they do not have prompt access to health care facilities and their standard of
living is often lower than that of the average Canadian.16 A lower standard of living is
linked to unhealthy behaviours such as smoking, eating mostly processed, high-salt, and
cholesterol diets.17 Indigenous people typically have heart attacks earlier in life than non-
Indigenous people. The 1801 Indigenous population has a higher prevalence of physical
inactivity, smoking, overweight, obesity, high blood pressure, and diabetes—all of which are
risk factors for cardiovascular disease and hypertension. Indigenous people are more likely
to have high blood pressure than the non-Indigenous population. As well, smoking rates
among Indigenous people are, on average, twice as high as those of non-Indigenous people
(39% versus 20.5%).18 New immigrants and primary hypertension. New immigrants to
Canada often have fewer chronic conditions upon arrival compared with the native-born
population. This trend is referred to as the healthy immigrant effect and reflects that fact
that when immigrants first arrive in their new homeland, they tend to be healthier than the
native-born population. However, new immigrants to Canada tend to experience a rapid
deterioration in their general health status after living in Canada for several years due to
lifestyle changes that impact their physical activity and dietary habits.19 Dietary
acculturation, which is the process by which immigrants adopt the dietary practices of the
host country, has been associated with obesity, diabetes, and hypertension.20 Dietary
acculturation for immigrant groups has largely been attributed to the “Westernization” of
immigrant diets, as characterized by an increased consumption of unhealthy north
American foods (e.g., fast food, junk food).20 In addition, immigrants may also be eating the
foods of their festivals (“festival foods”) more regularly. Festival foods are calorically rich
foods that are typically consumed only a few times a year, during festivals or special
occasions in the home country, and usually in limited amounts. After immigration,
immigrants tend to prepare the …Diseases of The Veins Summary