Blood Vessels






Figure 1.1


Normal artery, microscopic

This muscular artery in longitudinal section shows a thin intima (▪) above an imperceptible internal elastic lamina. Below this is the thick media (□), with layers of circular smooth muscle and interspersed elastic fibers to withstand the arterial pressure load and dampen the arterial pressure wave from left ventricular contraction. The media is bounded by the external elastic lamina (∗). Outside the media is the adventitia (▲), which merges with surrounding supporting connective tissue.



Figure 1.2


Normal artery and vein, microscopic

In cross-section a normal artery (▪) with a thick, smooth muscle wall lies alongside a normal vein (□) with a thin, smooth muscle wall and both traversing connective tissue in a fascial plane between muscle bundles of the lower leg. The larger arteries and veins are often grouped, along with a peripheral nerve, into a neurovascular bundle, to supply a body region. More distal areas with regional blood flow and the blood pressure are regulated by alternating vasoconstriction and dilation of small muscular arteries and arterioles.



Figure 1.3


Normal arteriole and venule, microscopic

A normal arteriole (▪) is alongside a normal venule (□) and a small peripheral nerve (+), all in cross-section, grouped into a loose neurovascular bundle. The major point of blood pressure regulation is at this arteriolar level. Exchange of solutes and gases with diffusion into tissues occurs at the capillary level. The diminished vascular pressure within venules, along with the intravascular oncotic pressure exerted by plasma proteins, mainly albumin, draws interstitial fluid back into the venules. Not seen here are the normally inconspicuous lymphatic channels that scavenge what little residual fluid is exuded from capillaries and not recovered into the venous system, preventing collection of interstitial fluid manifested as edema.



Figure 1.4


Atherosclerosis, gross

This is about as normal as an adult aorta can be. The intimal surface is quite smooth, with only occasional small, pale yellow, fatty lipid streaks visible (arrow) . Such fatty streaks may initially appear in children. (The faint reddish staining in this autopsy specimen comes from hemoglobin that leaked from red blood cells after death.) With a healthy lifestyle and without additional risk factors, these intimal fatty lesions are unlikely to progress. These lipid streaks may serve as precursors for atheroma formation. Major risk factors advancing atheroma formation include increased serum LDL cholesterol, decreased HDL cholesterol, hypertriglyceridemia, diabetes mellitus, hypertension, and smoking.



Figure 1.5


Atherosclerosis, gross

This coronary artery opened longitudinally shows irregularly shaped yellowish atheromatous plaques over much of its intimal surface. The focal dark red hemorrhage into a plaque is a complication of atherosclerosis that can acutely narrow the lumen. Endothelial dysfunction that impairs vasoreactivity or induces a thrombogenic surface or abnormally adhesive surface to inflammatory cells may initiate thrombus formation, promote atherosclerosis, and enhance vascular lesions of hypertension. Advanced atheromas can be complicated by surface erosion, ulceration, plaque rupture, hemorrhage, arterial aneurysmal dilation, calcification, and thrombosis. Arterial narrowing may lead to tissue ischemia, and marked or prolonged loss of blood supply may lead to infarction, with acute coronary syndromes involving the heart.



Figure 1.6


Atherosclerosis, gross

Severe aortic atherosclerosis involves nearly the entire intimal surface, with ulceration of the atheromatous plaques along with formation of overlying reddish-brown mural thrombus. This degree of atherosclerosis may develop over many years, or with significant risk factors driving more accelerated atherosclerosis, such as hyperlipidemia, diabetes mellitus, smoking, hypertension, and obesity. Mitigating these risk factors through adoption of a healthy lifestyle with increased exercise and reduced caloric intake can halt the progression of atherosclerosis, and atheromas can even regress over time, with reduced likelihood for complications.



Figure 1.7


Atherosclerosis, microscopic

This cross-section of aorta shows a large overlying advanced atheroma containing numerous thin, elongated cholesterol clefts, resulting from breakdown of lipid imbibed into foam cells. The luminal surface at the far left shows ulceration of its fibrous cap with hemorrhage. Despite this ulceration, which predisposes to mural thrombus formation, atheromatous emboli are not often clinically significant complications from them. The thick medial layer is intact, and the adventitia appears normal at the right. As atheromas enlarge, they can be complicated by ulceration, which promotes overlying thrombosis. Organization of the thrombus further increases the thickness and size of the plaque.



Figure 1.8


Atherosclerosis, microscopic

At high magnification the necrotic center of an aortic atheroma shows foam cells (□) and cholesterol clefts (▪). In the process of atheroma formation, endothelial injury leads to increased permeability, leukocyte adhesion, and release of cytokines that attract blood monocytes, which transform into tissue macrophages that accumulate lipids, becoming foam cells. Macrophages readily ingest oxidized LDL cholesterol through their scavenger receptors. Macrophages also generate cytokines, driving cellular recruitment. An increased serum LDL increases the amount of oxidized LDL, promoting this process. In contrast, HDL cholesterol tends to promote mobilization of lipid in an atheroma and transport out to the liver.



Figure 1.9


Atherosclerosis, microscopic

Marked coronary arterial narrowing results from smooth muscle cell migration and proliferation within the intima and media to form an enlarging fibrofatty atheroma, leaving just a small residual lumen. Shown here is a “complex” atheroma because of the large area of bluish calcification at the lower right with this H&E stain. Complex atheromas can have calcification, thrombosis, and/or hemorrhage. Calcification would make coronary angioplasty to dilate the lumen more difficult. Reducing the radius of an artery by half increases the resistance to flow 16-fold. When the degree of narrowing is 70% or more, angina is often present. Such patients are at great risk for acute coronary syndromes, including myocardial infarction and sudden death from dysrhythmias.



Figure 1.10


Atherosclerosis, microscopic

This coronary artery cross-section shows residual smooth muscle in the media with overlying atheroma composed of extensive lipid deposition in lipophages (□) and a cholesterol cleft (▪) from breakdown of those cells. These large plaques are prone to rupture, hemorrhage, and thrombosis. Platelets become activated and adhere to sites of endothelial injury, then release cytokines such as platelet-derived growth factor that promote smooth muscle proliferation, and the adherent platelet mass increases the size of the plaque, while narrowing the residual arterial lumen. Use of antiplatelet agents such as aspirin helps reduce platelet “stickiness” and slows their participation in atheroma formation.



Figure 1.11


Atherosclerosis, microscopic

This coronary artery cross-section shows severe occlusive atherosclerosis. The atheromatous plaque is circumferential and markedly narrows the remaining lumen. Note the prominent cholesterol clefts within this atheroma. This advanced atheromatous process involves the arterial media (▪) and the overlying intima (□). The remaining lumen has become occluded by a recent thrombus (∗) that fills it. Acute thrombosis is often the basis for acute coronary syndromes, including unstable angina, sudden death, and acute myocardial infarction. A thrombolytic agent administered urgently may aid restoration of blood flow.



Figure 1.12


Atherosclerosis, CT image

With contrast enhancement the aortic lumen (♦) is highlighted by bright attenuation of the blood, with darker gray mural thrombus seen around the periphery of the lumen. This slightly dilated abdominal aorta has severe atherosclerosis. Mural thrombus can form atop advanced atheromas, and thrombus can organize and narrow the lumen further, or portions may break off and embolize distally to occlude smaller arterial branches in the systemic circulation. This aortic wall also has focal thin, bright areas of atheromatous calcification. (The left kidney is absent from prior nephrectomy. The right kidney is brightly attenuated as intravenous contrast material flows through it.)



Figure 1.13


Atherosclerosis, angiogram

This patient’s poorly controlled type 1 diabetes mellitus for many years led to claudication (pain with exercise) in the right lower extremity. This angiogram reveals multiple areas of atherosclerotic narrowing (♦) involving femoral arterial branches. The upper leg with femur is in the left panel , and the lower leg with tibia and fibula is in the right panel . The arterial lumens appear dark with the digital subtraction imaging technique shown here.



Figure 1.14


Atherosclerosis, angiogram

There are multiple scattered pale areas representing atherosclerotic narrowing involving branches of the right femoral artery. This patient with poorly controlled diabetes mellitus developed severe peripheral vascular disease with claudication. On physical examination, peripheral pulses are decreased or even absent with this degree of arterial occlusion. The risk for tissue ischemia and possible gangrenous necrosis is increased.



Figure 1.15


Atherosclerosis, angiogram

The degree of atherosclerotic narrowing (♦) in this right internal carotid artery can lead to cerebral ischemia with mental status changes. Transient ischemic attacks could presage a subsequent stroke from ischemia to one or more areas of the brain. On physical examination, a bruit may be auscultated over such an area of large arterial narrowing, due to faster turbulent flow of blood distal to the region of narrowing (Bernoulli principle).



Figure 1.16


Hyaline arteriolosclerosis, microscopic

In addition to atherosclerosis, arteriosclerosis (hardening of the arteries) can encompass hyaline arteriolosclerosis, typically seen in kidneys and brain, and shown here involving the markedly thickened arteriole at the lower right of this glomerulus with PAS stain. This change often accompanies benign nephrosclerosis, leading to progressive loss of nephrons and eventual renal atrophy. Hyaline arteriolosclerosis is also seen in elderly individuals, who are often normotensive. More advanced arteriosclerotic lesions may occur in persons with diabetes mellitus (with nodular glomerulosclerosis seen here) and/or hypertension.



Figure 1.17


Hyperplastic arteriolosclerosis, microscopic

The hyperplastic form of arteriolosclerosis is prominent in this renal arteriole. It has an “onion skin” appearance from concentric, laminated intimal and smooth muscle proliferation with marked narrowing of the arteriolar lumen. Affected arterioles also may undergo fibrinoid necrosis (necrotizing arteriolitis), and there may be local hemorrhage. Surrounding tissues may show focal ischemia or infarction. This lesion is associated with hypertensive emergency, with systolic pressure ≥180 and/or diastolic pressure ≥120 mm Hg and signs of acute or ongoing end-organ damage such as encephalopathy, retinal hemorrhage, papilledema, or acute/subacute kidney injury. Hypertensive emergency may occur de novo or complicate long-standing, asymptomatic “essential” hypertension.



Figure 1.18


Medial calcific sclerosis, microscopic

Mönckeberg medial calcific sclerosis is a less significant form of arteriosclerosis (atherosclerosis and arteriolosclerosis are more significant because of greater risk for arterial luminal narrowing). It is more common in the elderly. Note the purplish blue calcifications involving only the media of this medium-sized artery; the lumen appears unaffected by this process. No significant clinical consequences occur in most cases, and it is usually an incidental radiologic imaging finding. Recall this process when you observe calcified muscular arteries on a radiograph of pelvic, neck, or breast regions.



Figure 1.19


Aortic aneurysm, gross

Atherosclerosis involving the intima and media may focally weaken the wall of the aorta so that it bulges out to form an aneurysm. A classic atherosclerotic aortic aneurysm typically occurs in the abdominal portion distal to the renal arteries, as shown here (∗). Aortic aneurysms tend to enlarge over time, and those with a diameter greater than 5 to 7 cm are more likely to rupture. Aneurysms may also form in the larger arterial branches of the aorta, most often the iliac arteries. On physical examination, there may be a palpable pulsatile abdominal mass with an atherosclerotic aortic aneurysm. Increased expression of matrix metalloproteinases that degrade extracellular matrix components such as collagen is observed in aortic aneurysms.



Figure 1.20


Aortic aneurysm, gross

This aorta sectioned longitudinally reveals a large abdominal atherosclerotic aortic aneurysm distal to the renal arteries (at the right) and proximal to the iliac bifurcation (at the left). This bulging 6-cm diameter aneurysm is filled with abundant layered mural thrombus (□). Note the rough atheromatous surface of the aortic lumen. The larger the aneurysm, the greater the risk for rupture.



Figure 1.21


Aortic aneurysm, CT image

An abdominal atherosclerotic aortic aneurysm (AAA) is located distal to the level of the renal arteries and can involve the branch point of the inferior mesenteric artery. Note the bright contrast material in the blood filling the open aortic lumen, whereas the surrounding mural thrombus (♦) has decreased (darker) attenuation. The total aortic diameter here is 7 to 8 cm, in great danger of rupture. A pulsatile abdominal mass was palpable in this patient. Although atherosclerotic aneurysms are more common in the abdominal aorta, they can also be found in the thoracic aorta. Ultrasound imaging is also useful for diagnosis of AAA.



Figure 1.22


Aortic dissection, gross

There is an intimal tear (arrow) located 7 cm above the aortic valve and proximal to the great vessels in this aorta with marked atherosclerosis. Risk factors for aortic dissection include atherosclerosis, hypertension, and cystic medial degeneration. When an intimal tear occurs, the systemic arterial blood under pressure can begin to dissect into the aortic media. From there, the blood may re-enter the aorta at a distal site through another tear, or it may dissect through the wall of the aorta and rupture into adjacent tissues or body cavities. Proximal ruptures may reach the pericardial cavity, with hemopericardium. There may be rupture into a pleural cavity, with hemothorax. With distal dissection, rupture into the abdominal cavity produces hemoperitoneum.



Figure 1.23


Aortic dissection, CT image ▶

Contrast enhancement highlights a dissection involving the aortic arch. The thin, dark linear segments (▲) mark extension of blood into the aortic media. There is extension of this dissection to involve the left common carotid artery. Aortic dissections may be diagnosed with CT, transesophageal echocardiography, MRI, or angiography. Angiography is preferred before surgical repair.



Figure 1.24


Aortic dissection, gross

The right common carotid artery is compressed by blood (♦) dissecting upward from a tear with aortic dissection. Blood may also dissect to involve the coronary arteries. Patients with aortic dissection may have symptoms of sudden, severe chest pain (with distal dissection) or may present with findings from proximal dissection that suggest a stroke (with carotid compression shown here) or myocardial ischemia (with coronary arterial compression). Pain may be absent in proximal dissections.



Figure 1.25


Aortic dissection, microscopic

This cross-section of aorta shows a red blood clot splitting the media and compressing the aortic lumen. This resulted from aortic dissection in which there was a tear in the intima of the aortic arch, followed by dissection of blood at high pressure out into and through the muscular wall to the adventitia. This blood dissecting out can lead to sudden death from hemothorax, hemopericardium, or hemoperitoneum. Severe knifelike chest pain may be present.



Figure 1.26


Aortic dissection, microscopic

The tear (arrow) in this aorta extends through the media, but blood also dissects along the media (∗). Medical management can be undertaken, but with leakage or rupture, surgical repair of the dissection can be performed with closure of the tear and placement of a synthetic graft, or endovascular stent.



Figure 1.27


Aortic dissection, gross

This thoracic aorta opened longitudinally shows an area in the thoracic portion of limited dissection that is organizing within the media. The red-brown thrombus can be seen on both sides of the section as it extends around the aorta. The intimal tear would have been at the left and the re-entry point at the right of the thrombus. This creates a “double lumen” to the aorta. This aorta shows severe atherosclerosis, which was the major risk factor for dissection in this patient.



Figure 1.28


Normal aorta, microscopic

This longitudinal section through the normal aorta with an elastic tissue stain shows the intima at the top. The thick aortic media shows parallel dark elastic fibers, here highlighted by the elastic stain. The smooth muscle fibers are between the elastic fibers, and both fibers give the aorta great strength and resiliency, allowing the pulse pressure of left ventricular systole to be transmitted distally. For a desirable normal young adult blood pressure of 90/60 mm Hg, the mean arterial pressure in aorta is 70 mm Hg.

Only gold members can continue reading. Log In or Register to continue

Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Blood Vessels
Premium Wordpress Themes by UFO Themes
%d bloggers like this: