What is the effect of oxidized low-density lipoproteins (LDLs) in atherosclerosis?
It causes smooth muscle proliferation.
Oxidized LDLs are toxic to endothelial cells, cause smooth proliferation, and activate further immune and inflammatory responses.
What is the primary mechanism of atherogenesis?
the release of toxic oxygen radicals that oxidize LDLs.
The oxidation of LDL is an important step in atherogenesis. Inflammation with oxidative stress and activation of macrophages is the primary mechanism.
What alteration occurs in injured endothelial cells that contributes to atherosclerosis?
They are unable to make the normal amount of vasodilating cytokines.
Injured endothelial cells become inflamed and cannot make normal amounts of antithrombotic and vasodilating cytokines.
What factor is responsible for the hypertrophy of the myocardium associated with hypertension?
Angiotensin II is also responsible for the hypertrophy of the myocardium and much of the renal damage associated with hypertension.
What pathologic change occurs to the kidney's glomeruli as a result of hypertension?
Ischemia of the tubule.
In the kidney vasoconstriction and resultant decreased renal perfusion cause tubular ischemia and preglomerular arteriorpathy.
Atherosclerosis causes aneurysm by?
Eroding the vessel wal.l
Atherosclerosis is a common cause of aneurysms because plaque formation erodes the vessel wall.
What is the usual source of pulmonary emboli?
Deep venous thrombosis.
Pulmonary emboli originate in the venous circulation, mostly from the deep veins of the legs, or in the right heart.
The differences between healthy vessel walls and those that promote clot formation is that there is , _____, of the endothelium of the vein.
Roughening of the endothelium of the artery and inflammation.
Exp: Invasion of the tunica intima by an infectious agent also roughens the normally smooth lining of the artery casing platelets to adhere readily. Anatomic changes of an artery can stimulate thrombus formation, particularly if the change results in pooling of arterial blood.
Which statement best describes thromboangiitis obliterates (Buerger disease)?
An inflammatory disorder of the small and medium-size arteries in the feet and sometimes in the hands.
Buerger disease is an inflammatory disease of the peripheral arteries. Inflammation, thrombus formation, and vasospasm eventually can occlude and obliterate portions of the small and medium-size arteries. Typically affect are the digital, tibial, and plantar arteries of the feet and the digital, palmar, and ulnar arteries of the hands.
Which of the following statements best describes Raynaud disease?
A basospastic disorder of the small arteries and arterioles of the fingers, and less commonly, the toes.
Raynaud phenomenon and Raynaud disease are characterized by attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes.
What changes in veins occur to create varicose veins?
Damage to the valves within veins.
If a valve is damaged, permitting backflow, a section of the vein is subjected to the pressure exerted by a larger volume of blood under the influence of gravity. The vein swells as it becomes engorged and surrounding tissue becomes edematous because increased hydrostatic pressure pushes plasma through stretched vessel wall.
The risk of developing coronary artery disease is increased up to threefold by:
Hypertension is responsible for a two- to threefold increased risk of atherosclerotic cardiovascular disease.
What is the usual source of pulmonary emboli?
Deep Venous Thrombosis.
Pulmonary emobli originate in the venous circulation, mostly from the deep veins of the legs, or in the right heart.
Which of the following can trigger an immune response within the bloodstream that can result in an embolus?
Amniotic fluid not only displaces blood, reducing oxygen, nutrient, and waste exchange, but also introduces antigens, cells, and protein aggregates that trigger inflammation, coagulation, and the immune response within the bloodstream.
Superior vena cava syndrome is a progressive ____ of the superior vena cava that leads to venous distention of the upper extremities and hand.
Superior vana cava syndrome, SVCS, is a progressive occlusion of the superior vena cava, SVC, that leads to venous distention in the upper extremities and head.
A local state in which cells are temporarily deprived of blood is defined as:
Coronary artery disease, CAD, can diminish the myocardial blood supply until deprivation impairs myocardial metabolism enough to cause ischemia, a local state in which the cells are temporarily deprived of blood supply. They remain alive but cannot function normally.
Nicotine increases atherosclerosis by the release of:
Nicotine stimulates the release of catecholamines, epinephrine and norepinephrine, which increases heart rate and causes peripheral vascular constriction. As a result blood pressure increases, as do cardiac workload and oxygen demand.
Which of the following is manufactured by the liver and primarily contains cholesterol and protein?
Low-density lipoproteins, LDLS.
A series of chemical reactions in the liver results in the production of several lipoproteins that vary in density and function. These include VLDLs, primarily TG and protein; LDLs, mostly cholesterol and protein; and HDLs, mainly phospholipids and protein.
Which elevated value may be protective of the development of atherosclerosis?
High-density lipoproteins, HDLs.
Low levels of HDL cholesterol also are a strong indicator of coronary risk, whereas high levels of HDLs may be more protective for the development of atherosclerosis than low levels of LDLs
Which lab test is an indirect measure of atherosclerotic plaque?
C-reactive protein, CRP.
Highly sensitive CRP, hs-CRP, is an acute phase reactant or protein mostly synthesized in the liver and is an indirect measure of atherosclerotic plaque related inflammation.
Cardiac cells can withstand ischemic conditions and still return to a viable state for how many minutes?
Cardiac cells remain viable for approximately 20 minutes under ischemic conditions. If blood flow is restored, aerobic metabolism resumes, contractility is restored, and cellular repair beings. If the coronary artery occlusion persists beyond 20 minutes, myocardial infarction occurs.
The scar tissue that is formed after a myocardial infarction, MI, is most vulnerable to injury between days:
10 to 14 days.
It is at this time in the recovery period, 10 to 14 days after infarction, that individuals feel more capable of increasing activities and thus may stress the newly formed scar tissue. After 6 weeks the necrotic area is completely replaced by scar tissue, which is strong but unable to contract and relax like healthy myocardial tissue.
What is the expected electrocardiogram pattern for a person when a thrombus in a coronary artery lodges permanently in the vessel and the infarction extends through the myocardium from the endocardium to the epicardium?
S T elevation, S T E M I.
These individuals usually have marked elevations in the ST segments on the E C G and are categorized as having S T E M I.
Angiotensin II increases the workload of the heart after a myocardial infarction by?
Increasing peripheral vascular resistance.
Angiotensin II also causes structural changes in blood vessels, remodeling, that contribute to permanent increases in peripheral resistance and make vessels more vulnerable to endothelial dysfunction and platelet aggregation.
Which of the following is a clinical manifestation of aortic stenosis?
The classical manifestations of aortic stenosis are angina, syncope, and heart failure.
Aortic and mitral regurgitation as well as mitral stenosis are caused by:
Mitral stenosis is most commonly caused by acute rheumatic fever, and is two to three times more common in women than in men. Acquired aortic regurgitation can be caused by rheumatic heart disease, bacterial endocarditis, syphilis, hypertension, connective tissue disorders like Marfan syndrome, and ankylosing spondylitis, appetite suppressing medications, trauma, or atherosclerosis.
A patient is diagnosed with pulmonary disease and elevated pulmonary vascular resistance. Which of the following heart failures may result from this condition?
Right heart failure.
Right heart failure is defined as the inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure. It most often results from the left heart failure, when the increase in left ventricular filling pressure that is reflected back into the pulmonary circulation is severe enough. As pressure in the pulmonary circulation rises, the resistance to right ventricular emptying increases.
Ventricular remodeling is a result of:
Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to inflammatory, immune, and neurohumoral changes that mediate a process called ventricular remodeling.
In systolic heart failure, what effect does angiotensin II have on stroke volume?
It increases preload and increases after load
Activation of the renin-angiotensin-aldosterone system, RAAS, cause not only increases in preload and afterload but also direct toxicity to the myocardium.
Impairs flow from the left ventricle.
Outflow obstruction increases pressure within the left ventricle as it tries to eject blood through the narrowed opening. Left ventricular hypertrophy develops to compensate for the increased workload.
Backflow into left ventricle.
During systole blood is ejected from the left ventricle into the aorta. If the aortic semilunar valve fails to close completely, some of the ejected blood flows back into the left ventricle during diastole.
Impairs flow from left atrium to left ventricle.
Mitral stenosis impairs the flow of blood from the left atrium to the left ventricle.
Backflow into the right atrium.
Tricuspid regurgitation is more common than tricuspid stenosis, and usually is associated with cardiac failure and dilation of the right ventricle secondary to pulmonary hypertension.
Backflow into the left atrium.
Mitral regurgitation permits backflow of blood from the left ventricle into the left atrium during ventricular systole, giving rise to a loud pansystolic murmur, throughout systole, heard best at the apex that radiates into the back and axillae .