ch.32 Flashcards

(67 cards)

1
Q

What is the leading cause of death worldwide?

A

Cardiovascular disease is the leading cause of death worldwide.

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2
Q

What is a varicose vein?

A

A varicose vein is a superficial vein in which blood has pooled.

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3
Q

Which veins do varicose veins typically involve, and what are their characteristics?

A

Varicose veins typically involve the saphenous veins of the legs and are distended, tortuous, and palpable.

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4
Q

What are the two causes of varicose veins?

A

Varicose veins are caused by (1) trauma to the saphenous veins that damages one or more valves, or (2) gradual venous distention caused by the action of gravity on blood in the legs.

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5
Q

How does the muscular pump in the legs normally function in relation to venous blood flow?

A

Normally the muscular pump in the legs moves venous blood up toward the heart, and valves prevent backflow and pooling of blood.

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6
Q

What happens to venous valves in individuals who habitually stand for long periods, wear constricting garments, or cross their legs at the knees?

A

In individuals who habitually stand for long periods, wear constricting garments, or cross the legs at the knees, distention progresses until the pressure in the vein damages venous valves, rendering the valves incompetent.

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7
Q

What effect do damaged valves have on venous pressure?

A

Damaged valves cannot maintain normal venous pressure, which causes hydrostatic pressure in the vein to increase.

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8
Q

What is chronic venous insufficiency (CVI), and how does it relate to varicose veins?

A

Varicose veins can progress to chronic venous insufficiency (CVI), which is defined as sustained inadequate venous return.

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9
Q

What is the pathological progression that leads from venous hypertension to ulceration?

A

Venous hypertension, circulatory stasis, and tissue hypoxia lead to an inflammatory reaction in vessels and tissue. This causes fibrosclerotic remodeling of the skin and then ulceration.

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10
Q

How does sluggish circulation to the extremities lead to venous stasis ulcers?

A

Circulation to the extremities can become so sluggish that the metabolic demands of the cells for oxygen, nutrients, and waste removal are barely met. Any trauma or pressure can therefore lower the oxygen supply and cause cell death and necrosis (venous stasis ulcers).

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11
Q

How does treatment of varicose veins and CVI typically begin, and what are examples of noninvasive treatments?

A

Treatment of varicose veins and CVI begins conservatively, and wound healing often occurs following noninvasive treatments, such as leg elevation, compression stockings, and physical exercise.

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12
Q

What are the new management techniques for treatment of varicose veins?

A

New management techniques include endovenous ablation (radiofrequency and laser) and ultrasound-guided foam sclerotherapy.

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13
Q

What are other management techniques for varicose veins that are less safe?

A

Other management techniques for managing varicose veins are surgical ligation and vein stripping, which are less safe.

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14
Q

What is a thrombus?

A

A thrombus is a blood clot that remains attached to a vessel wall.

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15
Q

What is a thromboembolus?

A

A detached thrombus is a thromboembolus.

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16
Q

Why are venous thrombi more common than arterial thrombi?

A

Venous thrombi are more common than arterial thrombi because flow and pressure are lower in the veins than in the arteries.

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17
Q

What is deep venous thrombosis (DVT), and what complication may result from it?

A

Deep venous thrombosis (DVT) refers to clot formation in the large veins, primarily of the lower extremities and may result in venous thromboembolism (VTE) to the pulmonary circulation.

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18
Q

What are the three factors (triad of Virchow) that promote venous thrombosis?

A

Three factors (triad of Virchow) promote venous thrombosis: (1) venous stasis (e.g., immobility, obesity, prolonged leg dependency <e.g., air travel>, age, heart failure <HF>), (2) venous endothelial damage (e.g., trauma, medications), and (3) hypercoagulable states (e.g., inherited disorders, malignancy, pregnancy, oral contraceptives, hormone replacement, hyperhomocysteinemia, antiphospholipid syndrome).</HF>

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19
Q

Who is at significant risk for DVT, and which hospitalized patients have particularly high risk?

A

Virtually everyone who is hospitalized is at significant risk for DVT, especially those with orthopedic trauma or surgery, spinal cord injury, and obstetric/gynecologic conditions.

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20
Q

When should inherited hypercoagulability states be suspected?

A

Inherited hypercoagulability states should be suspected in individuals who develop thrombi in the absence of the usual risk factors.

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21
Q

What leads to thrombus formation in the vein, and where does it often occur?

A

Accumulation of clotting factors and platelets leads to thrombus formation in the vein, often near a venous valve.

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22
Q

Why may a blood clot present as localized inflammation and swelling?

A

A blood clot may present as localized inflammation and swelling because the clot is causing backup and leaking into the surrounding tissues.

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23
Q

What typically happens to most thrombi, and what is the risk associated with untreated DVT?

A

Most thrombi eventually dissolve without treatment, but untreated DVT is associated with a high risk of thromboembolization of a part of the clot from the leg to the lung (pulmonary embolism).

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24
Q

What is post-thrombotic syndrome (PTS), and what proportion of individuals with DVT may develop it?

A

In up to one third of individuals with DVT, persistent venous outflow obstruction may lead to post-thrombotic syndrome (PTS), a frequent complication of DVT characterized by chronic, persistent pain; edema; and ulceration of the affected limb.

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25
Why is prevention crucial for DVT in at-risk individuals, and what are examples of prophylactic treatments?
Because DVT is usually asymptomatic and difficult to detect clinically, prevention for at-risk individuals is crucial. If possible, individuals should be mobilized as soon as possible after illness, injury, or surgery. Prophylactic treatment can include low-molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices.
26
What intervention may be necessary for individuals at high risk for pulmonary embolism when anticoagulation is contraindicated?
In individuals at high risk for pulmonary embolism, but for whom anticoagulation is contraindicated, placement of an inferior vena caval filter may be necessary to prevent pulmonary embolism.
27
How is diagnosis of a blood clot most often made?
Diagnosis of a blood clot is most often made by combining measurement of serum d-dimer concentration with lower extremity ultrasonography.
28
What is d-dimer as a diagnostic measure for thrombosis?
D-dimer is an indirect measure of the presence of thrombosis that is very sensitive but is not specific.
29
How is d-dimer interpreted in the diagnosis of DVT?
If the d-dimer is negative, DVT is ruled out. If it is positive, the diagnosis must be confirmed with ultrasonography.
30
What additional diagnostic methods may be needed for diagnosing a blood clot in selected individuals?
When it comes to diagnosing a blood clot in selected individuals, computed tomography (CT) or magnetic resonance imaging (MRI) may be needed to make the diagnosis. If noninvasive testing is nondiagnostic, a venogram may be indicated.
31
How is DVT treated?
DVT is treated with low-molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin.
32
When may thrombolytic therapy be used for DVT, and what are its benefits and risks?
Thrombolytic therapy may be used to dissolve the clot more quickly and reduce the risk of postphlebitic syndrome, especially when a large clot is located in a proximal vein. However, bleeding risk is increased, and many people have contraindications to the use of thrombolytics.
33
What is pharmacomechanical treatment, and what is its safety record?
Pharmacomechanical treatment involves catheter-mediated removal of clots that can be used in selected individuals and so far has a good safety record.
34
What is the recurrence rate of DVT after discontinuation of anticoagulant therapy, and how can it be reduced?
DVT has a recurrence rate of 26% 5 years after discontinuation of anticoagulant therapy, especially if it was unprovoked and no identifiable underlying condition can be reversed. In these individuals aspirin therapy can reduce recurrence rates after discontinuation of anticoagulants.
35
What is superior vena cava syndrome (SVCS)?
Superior vena cava syndrome (SVCS) is a progressive occlusion of the superior vena cava (SVC) that leads to venous distention in the upper extremities and head.
36
What is the leading cause of SVCS, and what are other causes?
The leading cause of SVCS is bronchogenic cancer (approximately 70% of cases), followed by lymphomas and metastasis of other cancers.
37
What are the benign causes of SVCS?
Benign causes of SVCS include thrombosis, histoplasmosis, tuberculosis, mediastinal fibrosis, cystic fibrosis, and benign tumors, such as retrosternal goiter.
38
What invasive therapies can lead to acute and chronic SVCS?
Invasive therapies, including pacemaker wires, central venous catheters, and pulmonary artery catheters, can lead to acute and chronic SVCS.
39
Why can the SVC be easily compressed by tissue expansion?
The SVC is a relatively low-pressure vessel that lies in the closed thoracic compartment; therefore, tissue expansion can easily compress the SVC.
40
How do cancers and lymph nodes contribute to SVC obstruction?
The right mainstem bronchus abuts the SVC so that cancers occurring in this bronchus may press on the vessel and obstruct venous return to the right atrium. Additionally, the SVC is surrounded by lymph nodes and lymph chains that commonly become involved in thoracic cancers and compress the SVC during tumor growth.
41
What are the clinical manifestations of SVCS?
Clinical manifestations of SVCS include edema and venous distention in the upper extremities and face, including the ocular beds.
42
What subjective complaints may individuals with SVCS report?
Individuals may complain of a feeling of fullness in the head, or tightness of shirt collars, necklaces, and rings.
43
What are other clinical manifestations of SVCS?
Other clinical manifestations include cerebral and central nervous system (CNS) 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.
44
How is diagnosis of superior vena cava syndrome made?
Diagnosis of superior vena cava syndrome is made by chest x-ray, Doppler studies, CT, MRI, and ultrasound.
45
Why is SVCS usually not a vascular emergency?
SVCS is not usually an emergency because of slow onset and the development of collateral venous drainage, SVCS is generally not a vascular emergency but rather an oncologic emergency.
46
What treatment options are available for SVCS related to malignant disorders?
Treatment for SVCS related to malignant disorders can include radiation therapy, surgery, chemotherapy, and the administration of diuretics, steroids, and anticoagulants, as necessary.
47
What treatment options are available for nonmalignant causes of SVCS?
Treatment for nonmalignant causes of SVCS may include bypass surgery using various grafts, thrombolysis (both locally and systemically), balloon angioplasty, and placement of intravascular stents.
48
What is hypertension?
Hypertension is consistent elevation of systemic arterial blood pressure.
49
Which population has among the highest rates of hypertension in the world?
Black adults have among the highest rates of hypertension in the world (44%).
50
How is hypertension defined in the Seventh Report of the Joint National Committee (JNC7)?
Hypertension is defined in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7) as a sustained systolic blood pressure of 140 mmHg or greater or a diastolic pressure of 90 mmHg or greater. This number changes often so look it up often.
51
What is isolated systolic hypertension (ISH)?
Isolated systolic hypertension (ISH) is elevated systolic blood pressure accompanied by normal diastolic blood pressure (less than 90 mmHg).
52
What is the prevalence trend of isolated systolic hypertension (ISH), and what is it associated with?
Isolated systolic hypertension (ISH) is becoming more prevalent in all age groups and is strongly associated with cardiovascular and cerebrovascular events.
53
What percentage of hypertension cases have no known cause, and what is this type called?
Approximately 95% of cases of hypertension have no known cause and therefore are diagnosed as primary hypertension.
54
What is secondary hypertension, and what percentage of cases does it account for?
Secondary hypertension accounts for 5% of cases and is caused by altered hemodynamics associated with an underlying primary disease.
55
What is hypertension as a complex disorder, and what risks are associated with it?
Hypertension is a complex disorder that affects the entire cardiovascular system, and all types and stages of hypertension are associated with increased risk for target organ disease events, such as myocardial infarction (MI), kidney disease, and stroke.
56
What factors are thought to be responsible for the development of primary hypertension?
A combination of genetic and environmental factors is thought to be responsible for the development of primary hypertension.
57
What is the nature of genetic predisposition to hypertension, and what systems are the inherited defects associated with?
Genetic predisposition to hypertension is thought to be polygenic. The inherited defects are associated with renal sodium excretion, insulin and insulin sensitivity, activity of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS), and cell membrane sodium or calcium transport.
58
What genetic variants are associated with hypertension and renal disease in blacks?
In blacks, variants of the apolipoprotein L1 (APOL1) gene are associated with hypertension and renal disease. This is why you always see in nursing textbooks that blacks are at high risk for cardiovascular disease.
59
What are the risk factors associated with primary hypertension?
Risk factors associated with primary hypertension include: (1) family history of hypertension; (2) advancing age; (3) gender (men younger than 55 and women older than 70 years); (4) black race; (5) high dietary sodium intake; (6) glucose intolerance (diabetes mellitus); (7) cigarette smoking; (8) obesity; (9) heavy alcohol consumption; and (10) low dietary intake of potassium, calcium, and magnesium.
60
What condition is characterized by hypertension, dyslipidemia, and glucose intolerance found together?
In fact, hypertension, dyslipidemia, and glucose intolerance often are found together in a condition called metabolic syndrome.
61
Why are low dietary potassium, calcium, and magnesium intakes risk factors for hypertension?
Although populations with high dietary sodium intake have long been shown to have an increased incidence of hypertension, recent studies indicate that low dietary potassium, calcium, and magnesium intakes are also risk factors because without their intake, sodium is retained.
62
How does nicotine in cigarette smoke affect blood pressure?
The nicotine in cigarette smoke is a vasoconstrictor that can elevate systolic and diastolic blood pressure acutely.
63
What are the long-term consequences of habitual smoking on cardiovascular health?
In habitual smokers an individual cigarette may not raise blood pressure, yet habitual smoking is associated with a high incidence of severe hypertension, myocardial hypertrophy, and death resulting from coronary artery disease (CAD).
64
How does alcohol consumption relate to hypertension incidence and cardiovascular mortality?
The incidence of hypertension is higher among heavy drinkers of alcohol (more than three drinks per day) than among abstainers, but moderate drinkers (two to four drinks per week) appear to have the lowest average blood pressures and cardiovascular mortality.
65
How is obesity recognized as a risk factor for hypertension?
Obesity is recognized as an important risk factor for hypertension, even in children and adolescents.
66
What causes hypertension?
Hypertension is caused by increases in cardiac output or total peripheral resistance, or both.
67
What is primary hypertension the result of, and what does it cause?
Primary hypertension is the result of a complicated interaction between genetics and the environment that increase vascular tone (increased peripheral resistance) and blood volume, thus causing sustained increases in blood pressure.