Blood vessel histology

Vasculitis

Students often focus on red blood cells when discussing the constituent cells circulating in the vascular network. However, blood vessels also carry leukocytes (white blood cells) that respond to infections as well as local injury. When cells are damaged (irrespective of the cause), resident phagocytes detect the damaged cells and release chemokines that attract more leukocytes from the microcirculation (chemotaxis). As a part of this inflammatory response, the blood vessels dilate in order to allow more white blood cells to gain access to the damaged site. Additionally, the epithelial cells of the blood vessels contract, creating spaces in the blood vessel wall through which leukocytes can migrate toward the injured tissue.

It is possible for an inflammatory cascade to be established in the walls of the vessels. This disorder is referred to generally as a vasculitis. The insulting factor may be infectious in nature (classically a Pseudomonas infection if bacterial, or Aspergillus if fungal) or non-infectious. The non-infectious subtypes are usually variants of an autoimmune characterized by any of the following:

• Immune complex deposition demonstrated in Systemic Lupus Erythematosus
• Antineutrophil cytoplasmic antibodies, which can be drug induced
• Antiendothelial cell antibodies, demonstrated in Kawasaki disease
• Autoreactive T-lymphocytes found in Giant Cell Arteritis.

Pathologically, damage to the blood vessels either by vasculitis or from malignant hypertension (for example) can result in fibrinoid necrosis. This is a special form of necrosis characterized by leakage of protein (such as fibrin) into the vessel wall. Consequently, the vessels appear bright pink on histological examination.

Atherosclerosis

Atherosclerosis is a disorder of the arterial vessels characterized pathologically by narrowing of the vessel lumen as a result of plaque deposition within the vessel wall. This should not be confused with arteriosclerosis, which refers to a general hardening and stiffening of arterioles and capillaries. Atherosclerosis is a subtype of arteriosclerosis and is often a complication of hyperlipidaemia that affects medium to large sized arteries, such as the coronary arteries (blood supply to the heart) or abdominal aorta.

There is widespread speculation surrounding the initiating factors behind atherosclerosis. However, one theory suggests that disruption of the endothelium of the vessel provides a nidus for lipoproteins (usually low density lipoprotein [LDL]) to accumulate in the tunica intima of the vessel. There are several confirmed insulting agents that can lead to endothelial damage. These include cigarette smoking, hypercholesterolemia and hypertension. Once in the intima, LDL becomes oxidized and will subsequently be engulfed by circulating macrophages. These macrophages are recruited to the site of injury and after engulfing the lipoproteins, they become foam cells.

At this point the lesion is known as a fatty streak and can be seen in patients in mid adolescence. In an attempt to prevent extravasation of blood, platelets accumulate at the site of endothelial injury and release more inflammatory mediators. The inflammatory markers promote the accumulation of more macrophages along with smooth muscle cells. The smooth muscle cells secrete extracellular matrix that (along with the smooth muscle cells and macrophages) form a fibrous cap. The core of the lesion may become necrotic and calcify. The plaque grows intraluminally, which can result in occlusion of the vessel. Furthermore, the plaque may become unstable and rupture, which would lead to embolization of plaque particles. The clinical manifestations of atherosclerosis depend on the vessels that are affected:

• Lesions of the coronary arteries would result in acute coronary syndrome (unstable angina, stable angina, ST-segment elevated myocardial infarction, non-ST segment elevated myocardial infarction, sudden cardiac death).
• Lesions of the mesenteric vessels can manifest as ischaemic bowel disease (acute or chronic mesenteric ischaemia, or ischaemic colitis).
• Lesions of the peripheral arteries (more commonly lower limb) will manifest as peripheral artery disease (characterized by lipodermatosclerosis, hair loss, nail changes and punched out ulcers).

Arteriovenous fistula

Typically, blood flows from arteries through capillary beds then to veins. There is a gradual decrease in intraluminal pressure progressing from arteries to veins. However, there are instances in which there are direct communications between arteries and veins. This abnormality is known as an arteriovenous (AV) fistula.

An AV fistula is often the result of surgically anastomosing an artery with a vein to facilitate dialysis of patients with chronic renal disease. However, there are cases of congenital AV fistulas that can arise at any point in the circulatory network. In iatrogenically created AV fistulas, there is hypertrophy of the tunica media that results in arterialization of the vein. This maturation process requires about three months before the access site can be used for dialysis. The maturation ensures that the vein becomes thick enough to tolerate repeated needle sticks.  

Vitamin C deficiency

Ascorbic acid (vitamin C) participates in a myriad of reactions within the body. Humans are unable to synthesize ascorbic acid and consequently depend on exogenous sources for this vitamin. One very important role of vitamin C is that it participates in the synthesis of collagen. Therefore, deficiency in vitamin C would result in underproduction of collagen. Recall that collagen is the chief component in the tunica adventitia of blood cells. This is the underlying cause of the bleeding of the gums seen in patients with scurvy.