Growth, smooth muscle cell growth and migration, platelet aggregation, thrombosis, endothelial dysfunction, and apoptosis
The potent vasodilator, bradykinin
Inhibition of renin
Brain, heart, adrenals, kidney, and the kidney’s efferent arterioles
Angiotensin-converting enzyme (ACE)
In the liver
More than 25 million Americans are affected by varicose veins.
Varicose veins are distended, tortuous, and palpable.
Habitually standing for long periods, wearing constricting garments, or crossing the legs at the knees can cause venous distention to progress.
The SNS has procoagulant properties, making vascular spasm and thrombosis more likely.
Altered connective tissue proteins, increased proteolytic enzyme activity, and decreased transforming growth factor-beta (TGF-β) in vein walls.
Multiple pathophysiologic mechanisms mediate these effects including the sympathetic nervous system (SNS), the RAAS, and natriuretic peptides.
The SNS contributes to the pathogenesis of hypertension by promoting cardiac contractility, heart rate, and inducing arteriolar vasoconstriction.
Additional mechanisms include structural changes in blood vessels (vascular remodeling), insulin resistance, increased renin and angiotensin levels, and procoagulant effects.
Venous thromboembolism (VTE) to the pulmonary circulation.
The sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS) are overactive in individuals with insulin resistance.
Secondary hypertension is caused by an underlying disease process that raises peripheral vascular resistance or cardiac output.
The focus is on the genetic, neurohumoral, and inflammatory mechanisms that underlie tissue and cellular processes.
Increased vascular volume is related to a decrease in renal excretion of salt, often referred to as a shift in the pressure-natriuresis relationship.
Increased SNS activity increases heart rate and peripheral resistance, causes vascular remodeling with narrowing and vasospasm of arteries.
Clot formation in the large veins, primarily of the lower extremities.
Chronic hypertension damages the walls of systemic blood vessels.
Leptin’s primary function is to interact with the hypothalamus to control body weight and fat deposition through appetite inhibition and increased metabolic rate.
Obesity is linked with insulin resistance, which affects vascular function and contributes to the development of sustained hypertension.
Numerous genetic vulnerabilities and environmental risks cause neurohumoral dysfunction and promote inflammation and insulin resistance.
It can lower the oxygen supply and cause cell death and necrosis (venous stasis ulcers).
A blood clot that remains attached to a vessel wall.
Primary hypertension is likely an interaction between many factors leading to sustained increases in blood volume and peripheral resistance.
Endothelial dysfunction, angiotensin II, catecholamines, insulin resistance, and inflammation contribute to the process.
Excess catecholamines raise vascular tone and increase peripheral resistance.
No, the pathophysiology of heart disease is much more complicated than just structural and hemodynamic changes.
Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance contribute to both increased peripheral resistance and increased blood volume.
Overactivity of the SNS can result from increased production of catecholamines (epinephrine and norepinephrine) or from increased receptor reactivity involving these neurotransmitters.
Inflammatory changes that affect autonomic innervation of veins.
Edema of the lower extremities and hyperpigmentation of the skin of the feet and ankles.
Blood pressure often declines even in the absence of antihypertensive drugs.
A shift in the pressure-natriuresis relationship is believed to be a central process in the pathogenesis of primary hypertension.
Disturbances in filtration and reabsorption of serum sodium, potassium, and calcium.
Disturbances in filtration and reabsorption of serum sodium, potassium, and calcium initiate the hemodynamics of early hypertension.
More than 900,000 incident or recurrent VTE events occur annually in the United States.
A varicose vein is a superficial vein in which blood has pooled.
Increased SNS activity causes increased heart rate and systemic vasoconstriction, thus raising the blood pressure.
Increased peripheral resistance and increased blood volume are two primary causes of sustained hypertension.
As sustained inadequate venous return.
Conservatively, with noninvasive treatments such as leg elevation, compression stockings, and physical exercise.
Yes, insulin resistance is common in hypertension even in individuals without clinical diabetes.
Decreased blood flow in distal areas initiates maximum peripheral resistance as an autoregulatory effort to adjust perfusion pressure.
Same as for Cushing syndrome.
Placement of an inferior vena caval filter may be necessary.
Increased SNS activity, insulin resistance, endothelial dysfunction, and procoagulant properties all contribute to sustained increases in blood pressure.
Venous hypertension, circulatory stasis, and tissue hypoxia.
Obesity.
Chronically high levels of leptin result in resistance to weight-reducing functions and increase sympathetic nervous system activity, decrease renal sodium excretion, promote inflammation, and stimulate myocyte hypertrophy.
Obesity-related changes result in vasoconstriction, salt and water retention, and renal dysfunction that may contribute to the development of hypertension.
Disturbance in filtration and/or reabsorption of serum sodium.
Excess catecholamines raise vascular tone and increase peripheral resistance.
Higher systemic blood pressure is required to maintain adequate cerebral perfusion.
Examples include immobility, obesity, prolonged leg dependency, age, and heart failure.
Virtually everyone who is hospitalized, especially those with orthopedic trauma or surgery, spinal cord injury, and obstetric/gynecologic conditions.
A venogram may be indicated.
Primary hypertension is the result of a complicated interaction between genetics and the environment that increase vascular tone (increased peripheral resistance) and blood volume, causing sustained increases in blood pressure.
The muscular pump in the legs normally moves venous blood up toward the heart.
They are as effective and safer.
Smooth muscle cells undergo hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media.
Adiponectin is a protein produced by adipose tissue but is reduced in obesity.
Impaired blood flow and renal ischemia invoke the compensatory renin-angiotensin-aldosterone mechanism to raise renal perfusion pressure.
Mucopolysaccharide deposits in vascular tissue increase resistance.
Loss of elasticity in vessel walls results in increased peripheral resistance.
Diagnosis is made by chest x-ray, Doppler studies, CT, MRI, and ultrasound.
New techniques such as renal denervation are being explored to treat hypertension.
Altered connective tissue proteins, increased proteolytic enzyme activity, and decreased transforming growth factor-beta (TGF-β) in vein walls.
Fibrosclerotic remodeling of the skin and then ulceration.
Insulin resistance affects renal function by causing renal salt and water retention.
The process is called vascular remodeling.
Microvascular dysfunction is linked to both the pathogenesis of hypertension and hypertension-related target organ damage.
They raise vascular tone and increase vascular resistance.
Genetic abnormalities include factor V Leiden mutation, prothrombin mutations, and deficiencies of protein C, protein S, and antithrombin.
Invasive therapies include pacemaker wires, central venous catheters, and pulmonary artery catheters.
Women are nearly twice as often affected by varicose veins as men.
Varicose veins are caused by trauma to the saphenous veins that damages one or more valves, or by gradual venous distention caused by the action of gravity on blood in the legs.
The SNS is implicated in the cardiovascular and renal complications of hypertension.
Insulin resistance and neurohumoral dysfunction contribute to sustained systemic vasoconstriction and increased peripheral resistance.
Chronic venous insufficiency (CVI).
A thromboembolus.
Medications are an important and often unrecognized cause of secondary hypertension.
Licorice contains glycyrrhizic acid, a mineralocorticoid that causes salt and water retention.
Processes such as endothelial injury, remodeling, stunning, reperfusion injury, and autoimmune disease are involved.
For a given blood pressure, individuals with hypertension tend to secrete less salt in their urine.
Efferent sympathetic outflow stimulates renin release, increases tubular sodium reabsorption, and reduces renal blood flow.
The SNS contributes to insulin resistance, which is associated with endothelial dysfunction and decreased production of vasodilators, such as nitric oxide.
It can become so sluggish that the metabolic demands of the cells for oxygen, nutrients, and waste removal are barely met.
The same sluggish circulation that impairs immune and inflammatory responses.
The interactions between obesity, hypertension, insulin resistance, and lipid disorders result in a high risk of cardiovascular disease.
Excess human growth hormone causes increased peripheral resistance.
Excess aldosterone promotes sodium retention and initiation of the hemodynamics of early hypertension.
They interface with neural control of blood pressure, initiating increased systemic blood pressure.
Inflammation around the thrombus promotes further platelet aggregation and thrombus propagation.
Cardiovascular disease is the leading cause of death worldwide.
Varicose veins typically involve the saphenous veins of the legs.
Valves in the veins prevent backflow and pooling of blood.
It becomes tortuous, and edema develops in the extremity.
Insulin resistance is associated with decreased endothelial release of nitric oxide and other vasodilators.
Obese individuals have been found to have hypertrophic remodeling of subcutaneous small arteries and endothelial dysfunction in response to acetylcholine.
Further studies may lead to new treatments for obesity-related hypertension.
Excess production of adrenocortical hormones promotes sodium and water retention.
Pathogenesis unclear.
Examples include inherited disorders, malignancy, pregnancy, oral contraceptives, hormone replacement, hyperhomocysteinemia, and antiphospholipid syndrome.
The valves become incompetent and cannot maintain normal venous pressure, causing hydrostatic pressure in the vein to increase.
Inflammation contributes to renal dysfunction, which, in combination with neurohumoral alterations, results in renal salt and water retention and increased blood volume.
Endovenous ablation (radiofrequency and laser) and ultrasound-guided foam sclerotherapy.
Because flow and pressure are lower in the veins than in the arteries.
Blood pressure returns to normal.
Decreased adiponectin is associated with insulin resistance, decreased endothelial-derived nitric oxide production, and activation of the sympathetic nervous and renin-angiotensin-aldosterone systems.
Possibly caused by sodium retention, plasma retention, weight gain, changes in levels and actions of renin, angiotensin, and aldosterone.
Inflammation around the thrombus may cause local symptoms.
Because poor circulation impairs the delivery of the cells and biochemicals for the immune and inflammatory responses.
The target organs for hypertension include the kidney, brain, heart, extremities, and eyes.
Increased inotropic effect on the heart elevates systolic pressure; diastolic pressure decreases due to decreased peripheral resistance.
Inherited hypercoagulability states should be suspected.
Computed tomography (CT) or magnetic resonance imaging (MRI) may be needed.
Respiratory distress may be present because of edema of bronchial structures or compression of the bronchus by a carcinoma.
Reduced blood flow and dysfunction of the organs perfused by these affected vessels is inevitable.
Elevated blood renin levels invoke elevations in angiotensin and aldosterone, causing blood pressure to rise.
Calcium ion directly affects vascular tonicity; elevated serum calcium levels increase vascular tone and peripheral resistance.
The three factors are venous stasis, venous endothelial damage, and hypercoagulable states.
The risk of bleeding is increased.
Benign causes include thrombosis, histoplasmosis, tuberculosis, mediastinal fibrosis, cystic fibrosis, and benign tumors.
71% of hypertensive adults are using antihypertensive medication.
ISH is strongly associated with cardiovascular and cerebrovascular events.
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.
ACE inhibitors and ARBs oppose the activity of the RAAS and are effective in reducing blood pressure and protecting against target organ damage.
Renal inflammation contributes to sodium retention and plays a role in the vascular dysfunction of hypertension.
Medications that block the RAAS include ACE inhibitors, direct renin inhibitors, Ang II receptor blockers (ARBs), and aldosterone inhibitors.
Glucocorticoids facilitate sodium and water retention, initiating the hemodynamics of early hypertension.
Approximately one third of VTE events are fatal.
Venous endothelial damage can be caused by trauma and medications.
DVT is treated with low-molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin.
SVCS is a progressive occlusion of the superior vena cava that leads to venous distention in the upper extremities and head.
Black adults have among the highest rates of hypertension in the world (44%).
ISH is elevated systolic blood pressure accompanied by normal diastolic blood pressure (less than 90 mmHg).
Risk factors include family history of hypertension, advancing age, gender, black race, high dietary sodium intake, glucose intolerance, cigarette smoking, obesity, heavy alcohol consumption, and low dietary intake of potassium, calcium, and magnesium.
Tissue ischemia causes inflammation of the kidney and contributes to dysfunction of the glomeruli and tubules, promoting additional sodium retention.
The best-known RAAS includes the release of renin, the synthesis of angiotensin II (Ang II) through angiotensin-converting enzyme (ACE), stimulation of the AT1 receptor (AT1R), and secretion of aldosterone.
Acute stress precipitates the release of catecholamines and glucocorticoids.
Increased pressure in the vein behind the clot may lead to edema of the extremity.
Because DVT is usually asymptomatic and difficult to detect clinically.
A negative d-dimer indicates that DVT is ruled out.
Headache, visual disturbance, and impaired consciousness.
Treatment may include bypass surgery using various grafts, thrombolysis (both locally and systemically), balloon angioplasty, and placement of intravascular stents.
Approximately 80% of hypertensive adults are aware of their condition.
High dietary sodium intake, low dietary potassium, calcium, and magnesium intakes are associated with an increased incidence of hypertension.
Overactivity of the RAAS in hypertensive individuals contributes to salt and water retention and increased vascular resistance.
Angiotensin II is associated with end-organ effects of hypertension, including atherosclerosis, renal disease, and cardiac hypertrophy.
Salt retention leads to water retention and increased blood volume, which contributes to an increase in blood pressure.
Increasing dietary intake of potassium, calcium, and magnesium can enhance natriuretic peptide function.
Ang II and aldosterone contribute to hypertensive hypertrophy and fibrosis of heart muscle, decreased contractility, and an increased susceptibility to arrhythmias and heart failure.
Hypertension may develop in an individual who routinely takes a monoamine oxidase (MAO) inhibitor with ingestion of a food containing tyramine, such as aged cheese.
By combining measurement of serum d-dimer concentration with lower extremity ultrasonography.
Aspirin therapy can reduce recurrence rates.
Because the SVC is a relatively low-pressure vessel that lies in the closed thoracic compartment.
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.
Arteriolar remodeling is a structural change in the vessel wall that results in permanent increases in peripheral resistance, mediated by angiotensin II.
Obesity is linked to inflammation, small artery remodeling, endothelial dysfunction, and insulin resistance.
Accumulation of clotting factors and platelets leads to thrombus formation in the vein.
With slow onset and the development of collateral venous drainage, SVCS is generally not a vascular emergency but rather an oncologic emergency.
The prevalence of hypertension is nearly equal between men and women.
Normal blood pressure is associated with the lowest cardiovascular risk.
A combination of genetic and environmental factors is thought to be responsible for the development of primary hypertension.
When there is inadequate natriuretic function, serum levels of the natriuretic peptides are increased.
Obesity causes changes in adipokines (leptin and adiponectin) and is associated with increased activity of the SNS and the RAAS.
Untreated DVT is associated with a high risk of thromboembolization to the lung (pulmonary embolism).
It involves catheter-mediated removal of clots.
Approximately 1 in 3 adults greater than 20 years of age has hypertension; this increases to nearly two thirds in those older than age 60.
Only 48% of those using antihypertensive medication have their hypertension controlled.
Secondary hypertension accounts for 5% of cases and is caused by altered hemodynamics associated with an underlying primary disease.
Cardiac output is increased by any condition that increases heart rate or stroke volume.
Obesity is recognized as an important risk factor for hypertension in both adults and children and contributes to many neurohumoral, metabolic, renal, and cardiovascular processes that cause hypertension.
PTS is a frequent complication of DVT characterized by chronic, persistent pain, edema, and ulceration of the affected limb.
Edema and venous distention in the upper extremities and face, including the ocular beds.
The recurrence rate is 26%.
Hypertension is defined as a sustained systolic blood pressure of 140 mmHg or greater or a diastolic pressure of 90 mmHg or greater.
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.
Peripheral resistance is increased by any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction).
Natriuretic hormones induce diuresis, enhancement of renal blood flow and glomerular filtration rate, systemic vasodilation, suppression of aldosterone, and inhibition of the SNS.
Endothelin blockade has been shown to reduce blood pressure and prevent proteinuria.
Research is under way to develop genetic and pharmacologic interventions that will stimulate the protective RAAS pathways.
Thrombolytic therapy may be used.
Cancers occurring in the right mainstem bronchus can press on the SVC.
Metabolic syndrome often includes hypertension, dyslipidemia, and glucose intolerance.
The RAAS provides an important homeostatic mechanism for maintaining adequate blood pressure and tissue perfusion.
Increased ANP and BNP levels in hypertension are linked to an increased risk for ventricular hypertrophy, atherosclerosis, and heart failure.
Abnormal amounts of Ang II contribute to insulin resistance, remodeling of blood vessels, and decreased release of endothelial vasodilators and anticoagulants.
A feeling of fullness in the head, or tightness of shirt collars, necklaces, and rings.
Treatment can include radiation therapy, surgery, chemotherapy, and the administration of diuretics, steroids, and anticoagulants, as necessary.
They are at risk for developing hypertension and many associated cardiovascular complications unless lifestyle modification and treatment are instituted.
Variants of the apolipoprotein L1 (APOL1) gene are associated with hypertension and renal disease in blacks.
Ang II causes systemic vasoconstriction and renal salt and water retention, and stimulates tissue growth and inflammation.
The leading cause of SVCS is bronchogenic cancer.
The SVC is surrounded by lymph nodes and lymph chains.
ISH is becoming more prevalent in all age groups.
Nicotine is a vasoconstrictor that can elevate systolic and diastolic blood pressure acutely.
Aldosterone contributes to sodium retention by the kidney and has other deleterious effects on the cardiovascular system.
Nesiritide is a drug that mimics the effect of natriuretic hormones and is used to treat heart failure.
In the kidneys, Ang II and aldosterone cause a shift in the pressure natriuresis curve, inflammation, and glomerular remodeling, contributing to renal failure in individuals with hypertension and diabetes.
Prophylactic treatments include low-molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices.
The diagnosis must be confirmed with ultrasonography.
The skin may become purple and taut, and capillary refill time is prolonged.
Hypertension is consistent elevation of systemic arterial blood pressure.
Habitual smoking is associated with a high incidence of severe hypertension, myocardial hypertrophy, and death resulting from coronary artery disease (CAD).
High levels of angiotensin II contribute to endothelial dysfunction, insulin resistance, dyslipidemia, and platelet aggregation, playing an important role in the complications associated with metabolic syndrome.
Natriuretic hormones modulate renal sodium (Na+) excretion and require adequate potassium, calcium, and magnesium to function properly.
Subtle renal injury results in renal vasoconstriction and tissue ischemia.
Endothelial injury and tissue ischemia result in the release of vasoactive inflammatory cytokines.
The second RAAS serves as a counterregulatory system, with ACE2 leading to the synthesis of angiotensin 1-7 from Ang II, which has vasodilatory, antiproliferative, antifibrotic, and antithrombotic effects.
Collateral venous drainage to the azygos vein usually has time to develop.
Approximately 95% of cases of hypertension have no known cause and are diagnosed as primary hypertension.
Obesity is recognized as an important risk factor for hypertension, even in children and adolescents.
The second RAAS uses ACE2 to create Ang 1-7, which has cardiovascular protective effects.
Endothelial injury and dysfunction in primary hypertension are characterized by decreased production of vasodilators like nitric oxide and increased production of vasoconstrictors like endothelin.
The second RAAS pathway is especially important in protecting renal tissue in those with diabetes and hypertension.
Hypertension is caused by increases in cardiac output or total peripheral resistance, or both.
The natriuretic hormones include atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and urodilatin.
Chronic inflammation contributes to vascular remodeling and smooth muscle contraction.
Angiotensin 1-7 stimulates Mas receptors and has vasodilatory, antiproliferative, antifibrotic, and antithrombotic effects, leading to lower blood pressure, less vascular inflammation and clotting, and decreased tissue remodeling and damage to target organ tissues.
