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Patho Ch23 Questions:

Terms in this set (17)

Thrombus formation: A thrombus is a blood clot that remains attached to a vessel wall. 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 (triad of virchow) promote venous thrombosis: (1) venous stasis e.g., immobility, age, congestive heart failure), (2) venous endothelial damage (e.g., trauma, intavenous medications), and (3) hypercoaguable states (e.g., inherited disorders, malignancy, pregnancy, use of oral contraraceptives or hormone replacement therapy). Persistent venous obstruction may lead to stasis ulcers of the affected limb.
Emboli: Embolism is the obstruction of a vessel by an embolus--a bolus of matter circulating in the bloodstream. The embolus may consist of a dislodged thrombus; an air bubble; an aggreagate of amniotic fluid; an aggregate of fat, bacteria, or cancer cells; or a foreign substance. An embolus travels in the bloodstream until it reaches a vessel through which it cannot fit. No matter how tiny it is, an embolus will eventually lodge in a systemic or pulmonary vessel determined by its source. Pulmonary emboli originate on the venous side (mostly from the deep veins of the legs) of the systemic circulation or in the right heart; arterial emboli most commonly originate in the left heart and associated with thrombi after myocardial infarction, valvular disease, left heart failure, endocarditis, and dysrhythmias. Embolism causes ischemia or infarction in tissues distal to the obstruction, causing organ dysfunction and pain. Infarction and subsequent necrosis of a central organ are life-threatening. For example, occlusion of a coronary artery will cause a myocardial infarction, whereas occlusion of a cerebral artery causes a stroke. Refer to table 23-3
Traumatic injury:
-Trauma to chest may allow air from lungs to enter vascular space
-Varicose veins: A vein in which blood has pooled; Distended, tortuous, and palpable veins (may be caused by trauma)
-Deep venous thrombosis:
Obstruction of venous flow leading to increased venous pressure (may be caused by trauma)
Atherosclerotic plaques: Atherosclerosis is a form of arteriosclerosis characterized by thickening and hardening of the vessel wall. It is caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a plaque. Atherosclerosis is not a single disease entity but rather a pathologic process that can affect vascular systems throughout the body, resulting in ischemic syndromes that can vary widely in their severity and clinical manifestations.
vasospastic disease: Thromboangiitis obliterans (Buerger disease) is characterized by the formation of thrombi filled with inflammatory and immune cells accompanying vasospasm. Over time, there thrombi become organized and fibrotic and result in permanent occlusion and obliteration of portions of small- and medium-sized arteries in the feet and sometimes in the hands.
Varicosites: Varicose veins (varicosities) are twisted, enlarged veins at the skin surface. The word comes from the Latin word varix, which means "twisted." Varicose veins occur due to poor functioning (malfunction) of valves in the deeper leg veins (venous insufficiency), making blood back up (pool) in the legs, with the resulting pressure causing surface veins to enlarge.
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. Causes include bronchogenic cancer (75% of cases), followed by lymphomas and metastasis of other cancers. Other less common causes include tuberculosis, mediastinal fibrosis, cystic fibrosis, and invasive therapies (pacemaker wires, central venous catheters, and pulmonary artery catheters).
Hypertension is consistent elevation of systemic arterial blood pressure.
Primary Hypertension: Primary hypertension is the result of an extremely complicated interaction of genetics and the environment mediated by a host of neurohumoral effects. Multiple pathophysiologic mechanisms mediate these effects, including the sympathetic nervous system (SNS), the renin-angiotensin-aldosterone system (RAAS), and natriuretic peptides.
Secondary Hypertension: Secondary hypertension is caused by an underlying disease process or medication that raises peripheral vascular resistance or cardiac output. Examples include renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), and drugs (oral contraceptives, corticosteroids, antihistamines). If the cause is identified and removed before permanent structural changes occur, blood pressure returns to normal.
Complicated Hypertension: As hypertension become more severe and chronic, tissue damage can occur in blood vessels and tissues leading to target organ damage in the heart, kidney, brain, and eyes. Cardiovascular complications of sustained hypertension include left ventricular hypertrophy, angina pectoris, heart failure, coronary artery disease, myocadial infarction, and sudden death. Myocardia hypertrophy in response to hypertension is mediated by several neurohormonal substances, including catecholamines from the SNS and angiotensin II. Hypertrophy is characterized by changes in the myocyte proteins, apoptosis of myocytes, and deposition of collagen in heart muscle, which causes it to become thickened, scarred, and less able to relax during diastole, leading to diastolic heart failure. In addition, the increased size of the heart muscle increases demand for oxygen delivery over time, the contractility of the heart is impaired, and the individual is at increased risk for systolic heart failure. Vascular complications include the formation, dissection, and rupture of aneurysms and atherosclerosis leading to vessel occlusion.
Isolated systolic hypertension (ISH): typically defined as a sustained systolic blood pressure (BP) reading that is >or= to 140 mm Hg and a diastolic BP measurement that is <90 mm Hg. ISH is becoming more prevalent in all age groups and is strongly associated with cardiovascular and cerebrovascular events.
The term orthostatic (postural) hypotension refers to a decrease in systolic blood pressure of at least 20 mm Hg or a decrease in diastolic blood pressure of at least 10 mm Hg within 3 minutes of moving to a standing position.
Patho: Normally when an individual stands, the gravitational changes on the circulation are compensated by such mechanisms as reflex arteriolar and venous constriction and increased heart rate. Other compensatory mechanisms include mechanical factors, such as the closure of valves in the venous system, contraction of the leg muscles, and a decrease in intrathoracic pressure. The normally increased sympathetic activity during upright posture is mediated through a stretch receptor (baroreceptor) reflex that responds to shifts in volume caused by postural changes. This reflex promptly increases heart rate and constricts the systemic arterioles. Thus, arterial blood pressure is maintained. These mechanisms are dysfunctional or inadequate in individuals with orthostatic hypotension; consequently, upon standing, blood pools and normal arterial pressure cannot be maintained.
symptoms: Orthostatic hypotension is often accompanied by dizziness, blurring or loss of vision, and syncope or fainting caused by insufficient vasomotor compensation and reduction of blood flow through the brain. Although no curative treatment is available for idiopathic orthostatic hypotension, often it can be managed adequately with a comination if nondrug and drug therapies--increasing fluid and salt intake, wearing thigh-high stockings, and taking mineralocorticoids and vasoconstrictors. Both acute and secondary forms of hypotension resolve when the underlying disorder is corrected.
Buerger: Patho: Thromboangiitis obliterans (Buerger disease) is characterized by the formation of thrombi filled with inflammatory and immune cells and accompanying vasospasm. Over time, there thrombi become organized and fibrotic and result in permanent occlusion and obliteration of portions of small- and medium-sized arteries in the feet and sometimes in the hands.
Symptoms: The chief symptom of thromboangiitis obliterans is pain and tenderness of the affected part, usually affecting more than one extremity. Clinical manifestations are caused by sluggish blood flow and include rubor (redness of the skin), which is caused by dilated capillaries under the skin, and cyanosis (a bluish discoloration of the skin) , which is caused by tissue ischemia. Chronic ischemia causes the skin to thin and become shiny and the nails to become thickened and malformed. In advanced disease, profound ischemia of the extremities resulting from vessel obliteration can cause gangrene necessitating amputation. Burger disease has also been associated with cerebrovascular disease (stroke), mesenteric disease, and rheumatic symptoms (joint pain).
Raynaud disease: Raynaud disease is characterized by attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes.
Patho: Raynaud disease is a common primary vasospastic disorder of unknown origin. Blood vessels in affected individuals demonstrate endothelial dysfunction with an imbalance in endothelium-derived vasodilators (e.g., nitric oxide) and vasoconstrictors (e.g., endothelin-1). Platelet activation also may play a role. It tends to affect young women and to consist of vasospastic attacks triggered by brief exposure to cold or by emotional stress. Genetic predisposition may play a role in its development.
Symptoms: The clinical manifestations of the vasospatic attacks of either disorder are changes in skin color and sensation cause by ischemia. Vasospasm occurs with varying frequency and severity and causes pallor, numbness, and the sensation of coldness in the digits. Attacks tend to be bilateral, and manifestations usually begin at the tips of the digits and progress to the proximal phalanges. Sluggish blood flow resulting from ischemia may cause the skin to appear cyanotic. Rubor, throbbing pain, and paresthesias follow as blood flow returns. Skin color returns to normal after the attack, but frequent, prolonged attacks interfere with cellular metabolism, causing the skin of the fingertips to thicken and the nails to become brittle. I severe, chronic Raynaud disease, ischemia can eventually cause ulceration and gangrene.
Peripheral artery disease (PAD) refers to atherosclerotic disease of arteries that perfuse the limbs, especially the lower extremities. PAD affects up to 20% of Americans ages 65 or older. The risk factors for PAD are the same as those previously described for atherosclerosis, and it is especially prevalent in individuals with diabetes. Lower extremity ischemia resulting from arterial obstruction can be gradual or acute. In most individuals, gradually increasing obstruction to arterial blood flow to the legs caused by atherosclerosis in the iliofemoral vessels results in pain with ambulation called intermittent claudication. If a thrombus forms over the atherosclerotic lesion, complete obstruction of blood flow can occur acutely, causing severe pain, loss of pulses, and skin color changes in the affected extremity. PAD is often asymptomatic in its early stages; therefore evaluation for PAD requires a careful history and physical examination that focuses on finding evidence of atherosclerotic disease (e.g., bruits), determining the ankle-brachial index, and measuring blood flow using noninvasive Doppler. Treatment includes risk factor reduction (smoking cessation and treatment for diabetes, hypertension, and dyslipidemia) and antiplatelet therapy. Symptomatic PAD should be managed with vasodilators in combination with antiplatelet or antithrombotic medications (aspirin, cilostazol, ticlopidine, or clopidogrel), cholesterol-lowering medications and exercise rehabilitation. If acute or refractory symptoms occur, emergent percutaneous or surgical revascularization may be indicated. Newer treatment modalities that are being explored include autologous stem cell therapies and angiogenesis.
Unstable angina: is the result of reversible myocardial ischemia and is a harbinger (warning sign) of impending infarction.
Myocardial infarction (MI): results when there is prolonged ischemia causing irreversible damage to the heart muscle.
Transient ischemia: ischemia lasting a short time
Sustained ischemia: ischemia lasting a long time
Stunned myocytes: a temporary loss of contractile function that persists for hours to days after perfusion has been restored.
Myocardial inflammation and necrosis: Myocardial infarction causes a severe inflammatory response that ends with wound repair. Damaged cells undergo degradation, fibroblasts proliferate, and scar tissue is synthesized. Many cell types, hormones, and nutrient substrates must be available for optimal healing to proceed. Within 24 hrs, leukocytes infiltrate the necrotic area, and proteolytic enzymes from scavenger neutrophils degrade necrotic tissue. The collagen matrix that is deposited is initially weak, mushy, and vulnerable to reinjury. Unfortunately, it is at this time in the recovery period (10 to 14 days after infarction) that individuals feel more like increasing activities and may stress the newly formed scar tissue. After 6 weeks, the necrotic area is completely replaced by scar tissue, which is strong but cannot contract and relax like healthy myocardial tissue.
Myocardial remodeling: a process mediated by angiotension II, aldosterone, catecholamines, adenosine, and inflammatory cytokines that causes myocyte hypertrophy and loss of contractile function in the areas of the heart distant from the site of infarction.
Refer to figure 23-16...Too much info read pg 604-609
Pericardial disease is a localized manifestation of another disorder, such as infection (bacterial, viral, fungal, rickettsial, or parasitic); trauma or surgery; neoplasm; or a metabolic, immunologic, or vascular disorder (uremia, rheumatoid arthritis, systemic lupus erythematosus, periarteritis nodosa). The pericardial response to injury from these diverse causes may consist of acute pericarditis, pericardial effusion, or constrictive pericarditis.

Acute pericarditis: Patho: Acute pericarditis is acute inflammation of the pericardium. The pericardial membranes become inflamed and roughened, and a pericardial effusion (escape of fluid) may develop that can be serous, purulent, or fibrinous. Possible sequelae (a condition that is the consequence of a previous disease or injury) of pericarditis include recurrent pericarditis, pericardial constriction, and cardiac tampondae (compression of the heart by an accumulation of fluid in the pericardial sac.)
Symptoms/evaluations: Symptoms may follow several days of fever and usually begin with the sudden onset of severe retrosternal chest begin with the sudden onset of severe retinosternal chest pain that worsens with respiratory movements and when assuming a recumbent position. The pain may radiate to the back as a result of irritation of the phrenic nerve (innervates the trapezius muscles) as it traverses the pericardium. Individuals with acute pericarditis also report dysphagia, restlessness, irritability, anxiety, weakness, and malaise. Physical examination often discloses low-grade fever (<38* C) and sinus tachycardia. A friction rub--a scratchy, grating sound--may be heard at the cardiac apex and left sternal border and is highly suggestive of pericarditis. The rub is caused by the roughened pericardial membranes rubbing against each other. Friction rubs are not always present and may be intermittently heard and transient. Hypotension or the presence of a pulsus paradoxus (a decrease in systolic blood pressure of >10 mm Hg with inspiration) is suggestive of cardiac tamponade, which can be life-threatening. Electrocardiographic changes may reflect inflammatory processes through PR segment depression and diffuse ST segment elevation without Q waves, and they may remain abnormal for days or even weeks. CT scanning and MRI may be used as diagnostic modalities.

Pericardial effusion: Patho: Pericardial effusion is the accumulation of fluid in the pericardial cavity and can occur in all forms of pericarditis. The fluid may be a transudate, such as the serous effusion that develops with left heart failure, overhydration, or hypoproteinemia. More often, however, the fluid is an exudate, which reflects pericardial inflammation like that seen with acute pericarditis, heart surgery, some chemotherapeutic agents, infections, and autoimmune disorders such as systemic lupus erythematosus.
Symptoms/evaluations: Pericardial effusion, even in large amounts, is not necessarily clinically significant, except that it indicates an underlying disorder. If an effusion develops gradually, the pericardium can stretch to accommodate large quantities of fluid without compressing the heart. If the fluid accumulates rapidly, however, even a small amount (50 to 100 ml) may create sufficient pressure to cause cardiac compression, a serious condition known as tamponade. The danger is that pressure exerted by the pericardial fluid eventually will equal diastolic pressue within the heart chambers, which will interfere with right arterial filling during diastole. This causes increase venous pressure, systemic venous congestion, and signs and symptoms of right heart failure (distension of the jugular veins, edema, hepatomegaly). Decreased arterial filling leads to decreased ventricular filling, decreased stroke volume, and reduced cardiac output. Life-threatening circulatory collapse may occur. An important clinical finding is pulsus paradoxus, in which arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10 mm Hg. Pulsus paradoxus in the setting of a pericardial effusion indicates tamponade and reflects impairment of diastolic filling of the left ventricle plus reduction of blood volume within all four cardiac chambers. The presence of large pericardial effusion or tamponade magnifies the normally insignificant effect of inspiration on intracardiac flow and volume. Other clinical manifestations of pericardial effusion are distant or muffled meart sounds, poorly palpable apical pulse, dyspnea (difficult or labored breathing) on exertion, and dull chest pain. A chest x-ray film may disclose a "water bottle configuration" of the cardiac silhouette. An echocardiogram can detect an effusion as small as 20 ml and is a reliable and accurate diagnostic test, although CT scans also may be done.

Constrictive pericarditis: Patho: In constrictive paricarditis, fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere, obliterating the pericardial cavity. The fibrotic lesions encase the heart in a rigid shell. Like tamponade, constrictive pericarditis compresses the heart and eventually reduces cardiac output. Unlike tamponade, however, constrictive pericarditis always develops gradually.
Symptoms/evaluations: Symptoms tend to be exercise intolerance, dyspnea on exertion, fatigue, and anorexia. Clinical assessment shows edema, distension of the jugular vein, and hepatic congestion. Restricted ventricular filling may cause a pericardial knock (early diastolic sound). ECG finding include T wave inversions and atrial fibrillation. Chest x-ray films often disclose prominent pulmonary vessels and calcification of the pericardium. CT, MRI, and transesophageal echocardiography are used to detect pericardial thickening and constriction and to distinguish constrictive pericarditis from restrictive cardiomyopathy. Pericardial biopsy may be needed to determine the etiology.
Cardiomyopathies: are a diverse group of diseases that primarily affect the myocardium itself. Most are the result of remodeling caused by the effect of the neurohormonal responses to ischemic heart disease or hypertension on the heart muscle. They may, however, be secondary to infectious disease, exposure to toxins, systemic connective tissue disease, infiltrative and proliferative disorders, or nutritional deficiencies. Many cases are idiopathic--that is, their cause is unknown. The cardiomyopathies are categorized as dilated (formerly congestive), hypertrophic, or restrictive depending on their physiologic effects on the heart (fig 23-25).

Dilated cardiomyopathy: is usually the result of ischemic heart disease, valvular disease, diabetes, renal failure, alcohol or drug toxicity, peripartum complications, genetic disorder, or infection. It is characterized by impaired systolic function leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure. Individuals complain of dyspnea, fatigue, and peripheral edema. Findings on examination include a displaced apical pulse, S3 gallop, peripheral edema, jugular venous distension, and pulmonary congestion. Diagnosis is confirmed by chest x-ray and echocardiogram, and management is focused on reducing blood volume, increasing contractability, and reversing the underlying disorder if possible. Heart transplant is required in several cases.

Hypertrophic cardiomyopathy: refes to two major categories of thickening of the myocardium: (1) hypertrophic obstructive cardiomyopathy (asymmetric septal hypertrophic cardiomyopathy or subaortic stenosis) and (2) hypertensive or valvular hypertrophic cadiomyopathy. Hypertrophic obstructive cardiomyopathy is the most commonly inherited cardiac disorder. It is characterized by thickening of the septal wall, which may cause outflow obstruction to the left ventricle outflow tract. Obstruction of left ventricular outflow can occur when heart rate is increased and intravascular volume is decreased. This type of hypertrophic cardiomyopathy is a significant risk factor for serious ventricular dysrhythmias and sudden death, and has been implicated in more than 33% of sudden deaths in young athletes. Hypertensive or valvular hypertrophic cardiomyopathy occurs because of increased resistance to ventricular ejection, which is commonly seen in individuals with hypertension or valvular stenosis (usually aortic). In this case, hypertrophy of the myocytes is an attempt to compensate for increased myocardial workload. Long-term dysfunction of the myocytes develops over time, with first diastolic dysfunction leading eventually to systolic dysfunction of the ventricle. Individuals with hypertrophic cardiomyopathy may be asymptomatic or may complain of angina, synocope, dyspnea on exertion, and palpitations. Examination may reveal extra heart sounds and murmurs. Echocardiography and cardiac catheterization can confirm the diagnosis.

Restrictive cardiomyopathy is characterized by restrictive filling and increased diastolic pressure of either or both ventricles with normal or near-normal systolic function and wall thickness. It may occur idiopathically or as a cardiac manifestation of systemic diseases, such as scleroderma, amyloidosis, sarcoidosis, lymphoma, and hemochromatosis, or a number of inherited storage diseases. The myocardium becomes rigid and noncompliant, impending ventricular filling and raising filling pressures during diastole. The overall clinical and hemodynamic picture mimics and may be confused with that of constrictive pericarditis.